NR1H4 and steatosis: Additionally, to further confirm the role of intestinal FXR in the effects of DC646 on MASH, we conducted in vivo efficacy evaluations in Fxr-deficient mice and found that the observed reductions in ALT levels and anti-steatosis effects in WT mice treated with DC646 were abolished in Fxr-deficient mice, demonstrating that the beneficial effects of DC646 on steatosis and MASH development are mediated through its specific targeting of intestinal FXR.