As the co-metabolites derived from host synthesis and microbial modification, bile acids can directly regulate the metabolic-dysfunction-associated steatohepatitis (MASH) through activating nuclear receptors including farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5), while indirectly shaping gut microbiota composition via modulating the intestinal epithelial microenvironment (17, –, 20). This evidence concerns the gene NR1H4 and metabolic dysfunction-associated steatohepatitis.