Taking the question as asked, rather than the general version of it. The liver data is among the strongest non-weight findings in the class. The semaglutide MASH programme reported a large advantage over placebo on MASH resolution, with a substantial minority also achieving fibrosis improvement — and fibrosis is the endpoint that predicts outcomes. Mechanistically it is reduced hepatic lipogenesis, increased fatty-acid oxidation, less hepatic inflammation, and possibly a direct effect on stellate-cell activation.

labquiet_amy said:

The liver data is among the strongest non-weight findings in the class.

That is correct as far as it goes, and here is where it stops going. Orforglipron is a small molecule rather than a peptide, which is the whole point: no SNAC absorption enhancer, no fasting window, no cold chain, and oral bioavailability in the tens of percent instead of around one. Phase 2 put it near 14.7% weight loss at 36 weeks on the top dose with a side-effect profile that looks like the injectables.

pete_nash said:

Reading the phase 2 write-up next to the injectable trials, and the comparison people keep making does not survive putting the two protocols side by…

Agreed, and ALT falling is not the same as fibrosis improving. Enzymes are a crude proxy; FIB-4 or elastography is what tells you about the thing that matters.

Adding the clinical framing, because it changes how the question reads. It helps to ask what evidence would change your mind before you look at any. If nothing would, the discussion is not about evidence, and it is better to say so early than to spend nine posts discovering it.