The figures, for anyone assembling their own picture. With resmetirom now available for MASH, combination approaches are being explored, so the standard of care in this area is moving faster than most threads assume.

One thing that is still open after Dr.NateNeph’s answer:

Whether normalised enzymes tell you anything about fibrosis, and what the right follow-up measurement is?

BiostatsBrad said:

With resmetirom now available for MASH, combination approaches are being explored, so the standard of care in this area is moving faster than most…

There is a second half to this that has not been said yet. 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.

Reporting back.

Update: the thing I was blaming turned out not to be the cause. Leaving the original post as written rather than editing it, so the mistake stays visible for whoever searches this next.

LindaRN_retired said:

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

Correct as far as it goes. The part it does not cover is what to do when the honest answer is "not enough data", which is more often than anyone likes.