Cancer is not one thing, it's a huge zoo of many many many ways that cells start to break the social contract and divide in an uncontrolled manner.
One of the most commonly observed broken mechanisms is mutation in the gene KRAS that turns this on/off growth switch into the permanently on position.
This has been known for decades, of course. And there have been huge amounts of effort to try to develop drugs that target KRAS in cancer, but for decades it's always been thought of as 'undruggable' because of the difficulty of finding any molecules that would affect it.
This new drug, that finally treats KRAS mutated cancers, goes about it in a new way. Instead of trying to gum up the works of a single protein by sticking a small chemical in it, it effectively "glues" the KRAS protein to another protein, CypA, which keeps the switch away from reaching the normal areas where it's "on switch" activity works.
So this new drug means two things: 1) a lot of the most difficult to treat cancers are now far more treatable, and in the next 1-5 years clinical trials will tell us which cancers this particular drug works well for, 2) there's an entire new class of drug activity that everybody is chasing at this very moment, so in 5-25 years we'll likely have a huge number more of these sorts of treatments.
How does it avoid targeting KRAS in healthy cells? Or is this another form of chemotherapy where we're trying our hardest to deliver the right amount of poison that kills the cancer before it kills the rest of you?
It doesn't. Cancerous cells have a much higher dependency on RAS signaling to survive, so it's a drug that kills everything that's replicating via RAS signaling, much like standard chemotherapy kills cells in general that are reproducing more quickly.
However this is just the first version of the drug, it can be combined with other modalities to allow more selective targeting of cancer versus not cancer cells (e.g antibody-drug conjugation). And when used in earlier stage cancers, rather than the advanced cancers in this first clinical trial, there's the possibility of lower dosing that has less strong side effects.
This is just the first attack that has ever broken through to hit a key weakness of some cancers. It's the start of learning, a breakthrough that will launch refinements, enhancements, and a ton of innovation. That sort of innovation is sometimes derided as "me-too" drugs, and not meaningful, but some of the biggest advancements in cancer care have been from taking very hard to tolerate treatments and making them more tolerable and refined and better for patients, allowing longer and more thorough killing of cancer cells. I would expect we will see a lot of that here, as well as work towards combinations with other drugs.
This drug targets cells with a KRAS mutation that locks the KRAS switch in the ON state, driving uncontrolled growth. Cells with this mutation are abnormal and predisposed to becoming cancer ... so by definition are not healthy.
>a lot of the most difficult to treat cancers are now far more treatable, and in the next 1-5 years clinical trials will tell us which cancers this particular drug works well for,
Can you help disambiguate this? Are there treatments now, or are there potential treatments with trials in 1-5 years?
The next 1-5 years will tell us which cancers this new drug will work well on, right now it's only been tried in pancreatic cancer when people have failed their first treatment. The new drug from the article, daroxonrasib, has nine trials i see currently, here:
The first two are the trial that just completed and showed success: people that have pancreatic cancer that failed other treatments, then a "trial" that is meant to give quick access to more people now that it's been shown to work.
Then there's a trial for using it as the first-line treatment for pancreatic cancer, one for lung cancer (NSCLC), and also various combinations with other drugs. I expect we'll see a ton of new trials registered in the coming year. Especially something in combination with colon cancer, because a common drug resistance mechanism in colon cancer is to develop KRAS mutation.
The thing is that we don't really know which cancers it will work well in until we try. And there's limited number of people with cancer that enter clinical trials, and we want to give each person their very best chance at survival, and then there's the massive expense of running the clinical trial itself, so learning happens slowly, one month of survival at a time, or one cancer recurrence at a time, or one death at a time. Patients that take part in clinical trials really are the heroes here. (Especially with the side effects of this new drug, which are horrible. It is a revolutionary drug, but we need to learn how to manage the other things it does as well, and that's going to take time.)
But that's not a cure. If they don't take that drug, assuming it works, they still have the original mutation in the cancer cells.
> Patients that take part in clinical trials really are the heroes here.
Are they?
To me personally, putting people into a permanent state of requiring drugs to survive, is not really cure. It's just maximizing income for those selling those drugs. And none of those drugs work exceedingly well; people still die, even if to other disease or frailties. I don't understand this hype in general.
I can understand being frustrated and cynical with the pharmaceutical industry, but I have never worked with a single doctor that approaches patient care with the goal of getting them "hooked" on something for life.
The pharmaceutical companies are not the ones making clinical decisions - in this case, it's a shared medical decision between a patient and their oncologist.
Having seen how horrific pancreatic cancer is, how difficult it is to treat, and the decades of slow research done by academic scientists to get to this point, I am elated that we have a tool to give patients more time with their families even if their cancer can't be "cured" with this particular drug.
This may seem unsatisfying, but it's real, measurable progress. KRAS has been known about since the earliest days of cancer research, so it's a true breakthrough to finally have a drug targeting it.
Pharmaceutical companies do make clinical decisions, it just isn't called a clinical decision. But they decide what research to pursue, and thereby decide which drugs exist for the doctor to choose.
They influence clinical decisions by adding to treatment options, but they do not make clinical decisions. If we believe that a drug's potential risks outweigh its benefits, clinicians will not prescribe it.
Wow, this is such a wildly pessimistic and cynical take. Are you okay?
> But that's not a cure. If they don't take that drug, assuming it works, they still have the original mutation in the cancer cells.
The person you're replying to called this out specifically:
> and also various combinations with other drugs.
Why do you think they try it in combination with other drugs? You might be right that this drug alone might not be a cure, but if it inhibits cancer growth, then it empowers other drugs to work more effectively.
> people still die
So what... We do nothing, then? This is your complaint? That we can't be immortal, so why bother trying to cure anything?
My wife died of aggressive melanoma. Immunotherapy would likely have helped her if not for some complications that delayed it.
Today, only 4 years later, there are two therapies, one RNA based and one CART that would have been usable in her situation. She’d be alive today most likely.
Frankly, you have no idea what you’re talking about as you spew toxic bullshit. 5 year survival would meant being there for her son through high school. That survival rate was 65% in 2022 and closer to 80% now in recent trials.
Normally I’d scroll on, but in these degenerate days it is important to counter bullshit before it becomes policy.
>However, even though the overall number of cases rises as the population grows, fewer people are getting and dying from cancer. Between 2000 and 2021, the incidence rate — or the rate of new cancer cases per 100,000 people — declined by 5.7%, while the annual mortality rate fell by 27.5%.
Cancer is a broad term encompassing many sorts of malfunction and nearly 40% of Americans will be diagnosed with it at some point because if you survive other hazards and maladies cancer is often what gets you.
This is just a failure of understanding. This particular advancement is part of a decades long slog which taken together allows a substantial number of people to live meaningful additional durations every single year. 6 months average by itself means that John got another 3 years even if Jane only got 3 more days.
If I pulled one person out of a burning building it would be newsworthy. Doctors are and have been pulling train loads every day.
I support doctors. They're doing great work. I understand that in today's US I probably should have said that explicitly, as many Americans seem to have joined the side of the cancer, viruses, etc., and now oppose doctors (or even blame doctors for the diseases). I'm not one of those irrational people.
I agree that 6 extra months (on average) means some patients get much more time than that. I agree that a statistically significant improvement on the survival rate for this terrible cancer is a very promising result longer term.
My disagreement was much narrower than that. I disagree that 6 extra months is equivalent to 5 extra years. I disagree that people living an extra 6 months on average is equivalent to one person living 3 extra years and one person living 3 extra days. I think 3 days and 3 years average out to about 1.5 years, not to 6 months.
Think of me as a living fossil who takes it for granted that everyone appreciates how much medicine improves our lives.
In my comment I pointed out that "5 years" was a bit of an exaggeration compared to the results in the article (6 months). That seemed unfortunate to me. To me 5 years seems much better than 6 months.
I think the meaning is that because we can see success with KRAS mutation of pancreatic cancer, we can now begin clinical trials for other cancers that may have KRAS mutation (colorectal, lung) and see if there is success there. If there is success in treating other cancers during clinical trials, it could be fast tracked through FDA to be more generally available and then become part of the national treatment option (ideally in 1-5 years after clinical trials).
Yes, and one of the hallmarks of cancer is a removal of the usual DNA damage checkpoints. Cells have sensors that detect damaged DNA and stop cell division, and once that is gone evolution happens on an extremely accelerated times scale. In lung cancer, for example, we have developed entire series of drugs to go after successive resistance mutations inside the EGFR gene.
When we first started getting good at sequencing the DNA of tumors, I remember initial reports of taking samples across the 3D space of a tumor and finding great spatial heterogeneity in the tumor genomes.
I'm actually most excited for using this drug in combination with colon cancer, where KRAS mutation is a common drug resistance evolution in response to drugs that target the gene EFGR (though cancer researchers may all have their favorites to go after, colon cancer went after my family especially hard).
Absolutely, this is selective pressure at work on cells with malregulated genetics. Most typically, this is in the form of drug efflux pumps, but you can definitely get more specific resistances.
Ways to avoid specific resistance include multiple treatments simultaneously, since the probability of generating resistance to both is the product of the probability of resistance either.
evolution is a wrong concept to approach it. cancer is not a separate life form, but a bug in the regeneration system of a complicated life form. it doesn’t exist outside of it, it cannot propagate.
Cancer researchers generally refer to it as evolution, and I've never heard any complaints from the population geneticists or evo-devo folks about it, so I don't think it's a tremendously controversial way to talk about it. See for example
The golden panacea for this would be a gene editing mechanism that will work in every cell in the body. Once we have something we can do whole hog gene replacement, most human health problems would be solved forever.
For every cell mechanism that's being abused by cancer to fuel its growth, there are other cells in the body for which that mechanism is crucial for their correct functioning. Wholesale editing every cell in the body mostly guarantees that the patient does not die of cancer -- the cure will kill them before the disease does.
No, a mechanism that acts on every cell on the body doesn’t mean it changes every cell. The primary problem with gene replacement therapies is they cannot be effectively delivered to every cell. If we can find a way to deliver to every cell than just the ones with the right signature will get the changes.
I don't much care what happens to most inmates but those with really long sentences should probably not be released early (or at all!) because they pose too much of a risk to the rest of us.
Until you get to the second order effects. If we want to find a cure for some disease, but we don't have enough people to do experiments on (maybe a lot of eligable prisoners died in previous trials) judges now have an incentive to hand out life sentences to people with that medical condition
Even just subconsciously that would have an effect
There’s literally nothing pointing towards this direction, rather the opposite.
Also the problem is not only judges, but the scope of detective work being done and when the crime was discovered etc. Judging comes last, but I guess we could deploy the infallible robot police squad which will do a flawless crime scene analysis etc.
I know this is a popular "well actually" to do, but it is not always useful in a conversation. Yes, all cancers are different, but yes, cancer is also one thing: unchecked, harmful division of cells.
Bacteria are also all different, but still they are "one thing", and despite their diversity, antibiotics exist that can deal with many species of them at once. It is reasonable to talk about bacteria and antibacterial medications, it is also reasonable to talk about cancer and cancer treatment. I truly hope cancer will meet its "penicillin" one day (yes I know this is unlikely).
It seems relevant here because the question was “How will this potentially help me if I get cancer?” and the answer is “Not at all unless you get a particular form of cancer that this applies to”.
> Bacteria are also all different, but still they are "one thing", and despite their diversity, antibiotics exist that can deal with many species of them at once.
Except people don’t ask “what if I get bacteria” the way they ask about cancer. If the story was about a new antibiotic that only affected 20% of common infectious bacteria strains and someone asked “in laypersons terms, how will this help me if I get a bacterial infection”, it would be appropriate to clarify that it only applies to some bacteria.
> Except people don’t ask “what if I get bacteria” the way they ask about cancer.
Yeah, but doctors also don't tell people "you have bacteria" or claim "we found a cure for bacteria". The lack of nuance on average is largely due to a lack of nuance from experts. The media treats cancer as one big thing and bacteria and viruses as separate things. Thus the average joe inherits 'treating cancer as one big thing' from the media.
I agree with you about the media. Cancer is often presented as a monolithic thing by the media. I don’t agree at all about experts. Doctors and scientists who research cancers do not lack nuance.
Oncologists are actually way more specific than even that. Because there are many forms of breast cancer and different treatments depending on the type.
But yeah, oncologists aren’t telling people “you have cancer” the way they might say “you have MRSA”.
Yeah, it's WAY more specific. We got a genetic breakdown, multiple pamphlets on the drugs being used, what they are targeting, and why they work (along with the risks).
Honestly, I think people probably get false impressions because cancer usually hits old people and old people are, frankly, often not reliable narrators.
I understand where you are coming from here, but I think it is helpful for people to overtly grasp that there are very different cancers, very different treatments, and indeed very different outcomes.
Without this understanding it becomes a quick jump from "we're spending all this money on cancer" to "we've made no progress"
An example of the nuance plays out in the common cancers (like breast and prostrate). These have between 90 and 100% 5 year survival rates. Others (like the one in this article, pancreatic) have very poor survivability.
As you note, it's very unlikely that we'll "cure cancer". But we already "cure" (for some definition of cure) some cancers. Progress is slow, methodical, and incremental. It can feel like a lost cause when viewed from afar, but up close very real progress is being made. And that's an important message to pass along.
The other part that is simply missing is that cancer, very unfortunately, evolves and mutates. That's how you go from a cancer that responds to treatment to one that is treatment resistant.
Like you said, for a lot of common cancers we have multiple treatments. It's usually not just one magic drug, but rather the doctors working with the most effective treatments down to the least effective treatments.
Depressing: evolution has discovered a universal cure for cancer, and it's reproduction. You make a whole new human without the bad bits. Other humans have to evaluate which bits are bad.
Which is why we got ecchemo.. where the cancer affected pathways get seperated from the regular ciculatory system via shunt and then get fed the chemo seperately and get a little wash before reconnection to the full circulation. It would be even more ideal if you had the whole navel setup in two entirely seperated systems.. sorry, a man can dream..
> We have penicilin that works against all human cells.
Penicillin works against bacteria, in particular gram-positive bacteria; to a lesser extent gram-negative bacteria too (this depends on the cell membrane structure of bacteria; there are other penicillin derivatives that are also more effective on gram-negative bacteria than penicillin is, but by and large the main target will be gram-positive bacteria). It does not work against human cells. If your comparison is about drugs in general, then of course cytotoxic drugs will have an effect; simplest example I can remember off-hand is colchicin. Of course it should work against cancer cells and non-cancer cells, unless there are some mutations where colchicin could no longer bind to, but that seems very very rare, due to the natural target of colchicin involved in cellular division.
It was an analogy. Just like penicillin kills a broad variety of bacteria we also know substances that kill a broad variety of cancer cells. Arsenic, for instance, and shotgun bullets. The problem is they usually select for all cells or all human cells, not cancer cells more specifically.
The correct way to read the sentence is “all cancers do not have the same causal mechanism” but people don’t talk like that because it’s off putting. Language is fluid and it’s generally on the reader to infer meaning from context. If we can do so reasonably, we do it, and we don’t need to then write additional posts chiding people over an interpretation that’s highly unlikely to be the intended one. I don’t mean to be pushy about this, btw. It’s just that pedantry can be valuable, but only if it isn’t abused.
Cancer cells, by definition, are not a uniform mass. It will depend on the cancer type, which in turn is defined by the properties those cells have. And mutations happen all the time, often more in cancer cells when their repair systems also have mutations, e. g. are less efficient. By that definition alone, there can never be a wonder-cure for all cancer types. At best you can find some proteins more important (p53 for instance) and while more than 50% of cancer cells have some form of mutation in p53, others simply don't. By that definition there will never be a penicillin-equivalent to all cancer types.
You're simply wrong. Again, cancer is malignant by definition. And again, you seem to be confusing "cancer" with "tumor" -- your description applies to the latter, not the former.
You can label a slow-growing tumor as "not-cancer" if you want, for psychological reasons, I guess; "cancer" just sounds scarier. Some slow-growing "not-cancer" tumors are faster than others. It's a sliding scale, not a dichotomy.
That's a link to a global chart. The OP is talking about the US. It's not surprising that countries that have to import natural gas are moving away from it and countries with plentiful local suppliew are doubling down on it.
Saying that this is more gas than coal is certainly not the case borne out by the numbers, even in the US, the one place where gas is as cheap as dirt due to it being a by-product of fracking.
Meanwhile solar and storage are continually plummeting in price.
So the current trend of approximately all new generation being renewables is going to accelerate. And then it will start eating into older, existing generation assets, causing early retirements of existing gas generation capacity.
Most investors think that any new gas generation built today will be a stranded asset long before its end of life. That doesn't matter to the hyperscalers, who run them so poorly and hard that the turbine shafts die in a few years and can afford it, but for regular utilities, buying any new gas generation is a boondoggle meant to soak the ratepayers and capture the guaranteed profit rate.
And the numbers above ignore residential solar, which will further lessen demand for gas, and as the cost of transmission and distribution soar on the grid, residential solar becomes an always better deal, because it skips all that.
The global cost-minimum for a future grid will have gas on it for maybe 20 more years, but not much after that. We'll switch to lots of storage and tons of over-capacity of solar and wind.
It will be interesting to see how solar evolves in the coming decade in US, maybe it could reach the current share of gas produced electricity, 40% . The country with the highest share of solar electricity is Hungary 27%, but they are part of the European electricity grid with lot of export and import.
Gas turbine manufacturing factories are very expensive and gas turbine manufacturers have already experienced turbine market crashed in 2018. Nobody wants to sit on loans for expensive idle factories in 5 years when the AI hype stops.
Per MWh costs of residential solar are usually 2x per MWh costs of utility scale solar. Utility scale solar power plants buy and install solar panels at larger scale and cheaper.
Most places can't run on residential solar + battery 365 days in year and need grid connectivity. As more homes install residential solar + battery the grid costs, which are independent of the number of hours when the grid is used, will stay the same. The amount of consumed gas will be lower. The costs of building gas power plants will stay the same (they are the backup), the costs of maintaining gas power plants will increase (more frequent ramping up and down).
"Ramping damage in gas turbines refers to the wear and tear or stress that occurs as a result of frequent changes in the operating load, also known as load cycling. Gas turbines are designed to operate efficiently at steady-state conditions, and deviations from these conditions can lead to various issues"
> Per MWh costs of residential solar are usually 2x per MWh costs of utility scale solar. Utility scale solar power plants buy and install solar panels at larger scale and cheaper.
The only problem with this comparison is the cost of the grid, which at least in the US will dwarf the savings from doing utility scale installs.
One nice thing about residential solar is that it greatly reduces the need for transmission, while perhaps requiring some short-term enhancement on distribution. And ideally dumping a bunch of storage at grid distribution nodes in the form of a container of batteries would solve a ton of problems and reduce costs a lot. This is of course heavily resisted by utilities because in most places in the US they make their money on T&D costs, so cutting those is a threat to their existence.
The US has literally double its total electricity production in solar and batteries stuck in the now 5 year FIFO permit hell we require for grid additions that will cause most proposals to pull out before completion
Yes, and this poor attitude of "safety" meaning "safe for the driver" extends to all sorts of terrible safety regulations.
41% of vehicle deaths are people not even in a car[1]. Yet car safety regulation is heavily focused on the 59% that are, nothing to regulate the ridiculous gender-affirming hood heights or aftermarket lifts that turn a survivable collision into a deadly collision.
It doesn't help your case when you state inflammatory remarks like "gender-affirming hood heights". This isn't reddit.
The data even points to the fact that, by total vehicles vs vehicles that cause pedestrian deaths, regular passenger cars cause 19.9 pedestrian deaths per 1MM registered vehicles while trucks, as and entire category, cause 19.2 pedestrians deaths per 1MM registered vehicles.
"nothing to regulate" is also an exaggeration. Many states to regulate aftermarket lifts. 6" lifts are typically the maximum legally allowed limit for trucks like the F150. You only see them higher because there is no enforcement of the rule.
> You only see them higher because there is no enforcement of the rule.
Unenforced rules effectively don't exist. Selectively enforced rules are a focal point for discrimination and corruption. I don't think you're making the argument you think you are.
> Yet all car safety regulation on the 59% that are
I don’t think you meant literally “all”, but one that comes to mind that definitely is intended for pedestrian safety is around requiring that EVs make audible noises when they’re moving at slow speeds (the fake humming as they move forward, and the beeping as they reverse).
This is one of the things I really like about driving a minivan. Excellent visibility compared to just about any other vehicle, including sedans. A combination of higher sitting position with larger windows and sloping hood really opens up sight lines. My son has a Mazda 2 and I hate driving that thing. Feels like the columns and ride height really kills visibility.
100%. I have a Mazda cx-5. Visibility sucks looking left & right because the A frame is so thick.
My thought: demand a certain level of visibility from car manufacturers, and they can figure out how to design around it. Like, I must be able to look left and see the pedestrian 3 feet away from walking into my car. Blind spots like that in the front are ridiculous
How often do you come across kids sitting on the ground in a parking lot? If they want to make a point about visibility at least have them standing up.
Yup, and I still don't know how she was able to do that, knowing that he was there. If you know that you can't see well out of your vehicle, make sure the kids aren't anywhere near it when you're driving. Hell, when my kids were young, they weren't even allowed to be outside on the same side of the house that I was mowing.
Not sure if you have kids but it's pretty terrifying to navigate through parking lots with toddlers. It's the most stressful part of my day, honestly. And yet what choice do I have in the US but to put up with it? Safer city planning is pretty much banned except for the most expensive places in the US.
However I think your EV examples shows an important attitude about what types of vehicles can be regulated. EVs are fair game for regulation, oversize trucks and SUVs are not. That's an attitude not based on safety, but on societal priorities.
This two-class system extends even beyond safety regulations, into emissions regulations too. Trucks and oversize SUVs get a free-ride out of everybody else in society.
> The results were striking: compared to traditional fat-tree networks, RNG (Resilient Network Graphs) uses 69% fewer routers, delivers 33% higher throughput, cuts network power by 40%, and lowers operating costs by 27. In early 2026, RNG became the default design for most newly built Amazon data centers globally.
> For cabling, they developed the ShuffleBox—a passive optical device whose internal wiring combined with randomized ShuffleBox-to-ShuffleBox cabling yields “quasi-random” graphs that behave like truly random graphs.
This is pretty incredible, random layouts of networks that have on-average better properties...
I'm really curious about the long tail of performance though. What is the worst case scenario here? And are there some better case scenarios? Uniformity in Clos networks is pretty great, but many loads don't need uniformity, and if these RNG-based networks have non-uniformity, perhaps that has operational characteristics that can be helpful or harmful.
"Performance guarantees are stochastic rather than deterministic. The worst case performance (for metrics such as number of hops and oversubscription) is known, but for RNG our models are stochastic (i.e., the worst case performance is known with high probability). This is a weaker limitation than it might appear. Fat-tree guarantees are also effectively stochastic once you account for real-world failures, which are frequent at scale. RNG simply makes the stochastic nature explicit and designs for it from the start."
Well I guess I'd like to see those guarantees, but more specifically, the variance of them.
I think Section 9, and Figures 13/14 in the Arxiv preprint sort of address this, but it doesn't mention anything about accounting for real-world failures in fat trees. I haven't had a chance to read it all, though...
We can print more money, but it's not about "affording" it, the money printing at most changes the value of the dollar (i.e. inflation/deflation).
The rest of the world wants dollars, and as long as they do, the US benefits massively from that demand, and it would be foolish not to satisfy that demand, as it's pure benefit to the US.
It seems that many are devoted to ending the status of the dollar as the reserve currency of the world, but it's a strange and subversive thing for any US resident to want or desire.
I think there's a reasonable question of whether the Siri stuff is even a feature that customers want. Additionally, money can not solve all problems, 9 people can't make a baby in a month, and if these sorts of regulations are serious at all like they are for medical regulation then you really do need to do the work of assessing risks, etc., and there's a chain of waterfall development to all that.
Let's go check on the cautionary tales of the Tesla shorts.... poor folks, we let them run around in the yard of the asylum without a fence because they have lost the motivation even to run away. They just keep mumbling about PE ratios....
From my perspective it's more of a "stay away" type of stock (short or not). The price is not supported by business finance fundamentals, and seems to be pushed upward via the retail market, driven by Elon's gift for selling futurism to the masses. To me, the value of Musk's companies is dangerously dependent on one single person, in a way that I can't think of for any other current company. It makes "investment" in the company more speculative, and closer to other "retail mass" phenomena like "meme stocks" or cryptocurrency.
As an example here, in the 2022 (relatively mild) stock market downturn, when the S&P 500 gave back about 20%, TSLA dropped from a peak in the low 400s, to a low of 122... roughly a 70% drop peak to peak. It's back to ~400 now, and it could go higher again. But, in the next downturn, it could go a lot lower.
Very little of the IPO is related to anything government, or space for that matter. It's mostly a rental service for some GPUs that were hoarded, with the promise that somehow in the future the $2B/month that Anthropic and Google are paying SpaceX for compute infrastructure will somehow grow, that somehow SpaceX will grab valuable GPU real estate before others and continue renting it to others who actually make productive services.
Anti-immigration policy blocks them from being Americans.
I know an awful lot of skilled people that live in the US, pay high taxes, and for whose lives have been thrown into disarray by backwards, anti-immigration policy like this illegal $100k fee, but it's just the beginning of the ways that anti-immigration policy is being used to make the US far weaker, just in order for pyrrhic harm to immigrants. I'm pissed about it.
>Anti-immigration policy blocks them from being Americans.
Yes, because the citizens of a country (through their elected representatives) have absolute control over who they choose to allow into their country. Even blocking a brilliant surgeon or inventor, if they so choose. There is no moral right to come to America (or any other country).
Saying "I have absolute control" is not a justification for making bad decisions that hurt the US. Furthermore, it was never a question of the US had a right to make these decisions, of course it does.
Do you find the argument "I have the right to make any decision I want therefor it justifies bad decisions" convincing? I sure don't.
>Saying "I have absolute control" is not a justification for making bad decisions that hurt the US.
How is it a bad decision that will hurt the US? Can you make that argument on its merits? No one doubts that there isn't that one genius here or there
Last year, right here on HN I saw a headline where the "powers that be" wanted to increase Canada's population to 100 million (they currently sit at 30ish million). Is that a good decision for Canada? Where the fertility rate is so low population is shrinking? Like, do they need another 65 million people? Are there 65 million jobs going undone in Canada right now? Jobs that desperately need doing? The plan's the same for the United States, even if no one was careless enough to blare a similar headline from trumpets.
That's false. You can apply for an H1B while in the US (unless there has been another recent and random change to long standing policy for no reason except to make lives miserable).
H1B renewals are also common, and happen within the US.
One of the most commonly observed broken mechanisms is mutation in the gene KRAS that turns this on/off growth switch into the permanently on position.
This has been known for decades, of course. And there have been huge amounts of effort to try to develop drugs that target KRAS in cancer, but for decades it's always been thought of as 'undruggable' because of the difficulty of finding any molecules that would affect it.
This new drug, that finally treats KRAS mutated cancers, goes about it in a new way. Instead of trying to gum up the works of a single protein by sticking a small chemical in it, it effectively "glues" the KRAS protein to another protein, CypA, which keeps the switch away from reaching the normal areas where it's "on switch" activity works.
So this new drug means two things: 1) a lot of the most difficult to treat cancers are now far more treatable, and in the next 1-5 years clinical trials will tell us which cancers this particular drug works well for, 2) there's an entire new class of drug activity that everybody is chasing at this very moment, so in 5-25 years we'll likely have a huge number more of these sorts of treatments.
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