And then the fact that both of them work is just strong evidence for that underlying hypothesis being correct, right? That hypothesis, liver fat is toxic, and so if you reduce it in whatever way you can, if we reduce that fat, we can reverse inflammation and even fibrosis, which is a pretty remarkable validation for that excess fat toxicity model.

By and large, the person with MASH, with F2 or F3 fibrosis, what that person really needs is a resolution of the underlying condition that led their liver to be sick in that way, and that's why weight loss is number one, through whatever means possible.

If it happens through diet, fantastic.

If it happens through bariatric surgery or pharmacologic therapy, also awesome.

And then in sequence, if that person still has a high risk for cirrhosis or F3 fibrosis, then it's a person that definitely needs one of these liver-directed therapies, the resmetiroms, the efruxiferm.

You'll have some people advocate that you can use both drugs in combination, right? But, uh, again, our goal is to reduce overall morbidity and mortality.

It begins with treating the underlying cause, the insulin resistance, the cardiovascular risk.

I mean, this makes me think a lot about the future of MASLD.