Answering the narrow version, because the broad one does not have a single answer. 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.

DanielChem_CHI said:

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

Agreeing with DanielChem_CHI, and the qualification matters more than the agreement. 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.

If somebody has the primary source to hand I would rather cite it than paraphrase it.

Dr.EM_Chicago said:

I have been following the oral non-peptide data since phase 2 and I am trying to work out how much of the enthusiasm here is about efficacy and how…

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.

Clinical perspective, offered as context rather than as advice. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.