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.

A narrower follow-up, since the general answer is now clear:

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

quinn_sf 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…

Coming at quinn_sf’s question from a different direction. 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.

OP back with an update, since a thread like this is useless without one.

Resolved, and the thing that resolved it was the least interesting suggestion in the thread. Writing that down for the next person who wants the interesting answer.

pete_nash said:

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

Right, and the exception is worth naming rather than left implied, because the exception is where people get into trouble.