The side effect of pytor, statins are really, really bad. For a large number of patients, you and you know, even moderate dose statins, you have a percentage of the patient population, that's probably under 20%. I'm not sure what the number actually is, but it's about there who just can't use that ends, because they just they just isn't good for them. Further, whatever you do with blood cholesterol, if you have lipid Laden, soft Clark, they just really aren't many good options. Getting rid of those blocks just isn't isn't on the table, there really isn't much you can do. So we need a better way of going forward. And yet, and yet, if you look at like, you know, what is the one of the latest $3 billion companies that are out there just going public, what are they doing? They're lowering LDL cholesterol, if you look at like the latest therapies where they're planning to charge half a million dollars a year. For these for these high tech therapies, what are those therapies doing? They're finding new ways to lower LDL cholesterol, it's not a good environment. What are the alternatives? So let's start with the ones that don't work. As you as you might recall, I mentioned you know, inflammation is a big problem here. But if you reduce inflammation, systemically using the approaches that are available now, studies suggest that you get about the same benefit as you do from lowering LDL cholesterol, which isn't to say that somebody couldn't come up with a way of doing this better. And in a more targeted fashion, that actually works. For some definition of works. But the tools that are available to reduce systemic inflammation are just not, they're pretty blunt right now. And they just don't do enough. I think there was a study I was looking at recently, which shorts showed an 8% sort of reversal a plot which just isn't, isn't good enough. So alternative number two, which seems much more much better, you know, as soon as your as soon as you'd go to your ceiling are much better as mice. So reverse cholesterol transport is the part where your macrophage sucks up the cholesterol hands it off to the bloodstream. And there's a number of genes are involved in this, this this sort of block diagram here. These if we imagine these blue things are macrophages, what they're doing is they use abca. One to handoff to an HDL particle initially, and then ABC, g one helps you add more cholesterol to the particle, the particle heads back to the level where it's picked up. Next threaded into, into and you know, objective from the body. This way, anything you do pretty much anything you do in mice to make one part of this system or more parts of the system work better, you can upregulate abca, one, you can put more HDL particles, you can make macrophages consume more cholesterol, it all works great in mice even use, some of the methods have achieved 50% reversal plock limits, which is amazing. And should cars correspond to roughly a 50% reduction in mortality. But every time they tried to do something in humans, they fail. There's a whole list of clinical trials that have failed over the last 20 years trying to improve the various cholesterol transport or things that work really well in mice. So what that tells us is that we do not understand something very important about the way in which cholesterol transport is rate limited in its different steps in humans versus in mice. So anybody trying to do something here, I wish them luck. But the odds are not good based on based on historical, historical efforts. So my position our position at repair is the position of a number of other people is that the true path forward is stopped macrophages, exploding the world, make them resilient to the environment they find them in, in all tissues. So if they can just be made to not do the crazy things they do when they're exposed to you know, oxidized cholesterol and LDL particles and and systemic inflammation, then great. In theory, if they can keep doing what they did when they were useful, they will just dismantle clock over time. And atherosclerosis were worse because that's what these cells are meant to do. And it's what they do do if they're not being if they're not being trampled by by the circuit. stances of being old.