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.

Dr.KarenChen said:

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

Dr.KarenChen has the substance of this right. The condition it depends on is worth stating. The manufacturing argument is the underrated one. Peptide synthesis capacity has been the binding constraint on this entire class, and a small molecule is made in ordinary chemical plants. If it holds up in phase 3, the supply and price picture changes more than the efficacy picture does.

hank_denver 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. The mechanism and the magnitude are separate questions. Agreeing that something happens says nothing about whether it happens enough to act on.

I would rather be corrected than agreed with, if it comes to it.