Short answer first, then the reasoning. 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.

JessicaH_TX said:

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

No disagreement with JessicaH_TX. One condition attached. 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.

PurityPaulOR 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.

Adding the clinical framing, because it changes how the question reads. Worth answering the question that was asked rather than the one behind it. The narrow version usually has an answer; the broad version usually does not, and answering the broad one is how a thread stops being useful.

Ask again with the specifics and you will get a better answer than this one.