That is, the intestinal flora can regulate the occurrence and development of NAFLD through bile acid metabolism and farnesoid X receptor (FXR)/ endogenous takeda G-protein-coupled receptor 5 (TGR5) signal transduction pathways, which play key roles in controlling the de novo synthesis of fat in the liver and the transport of triglycerides. The gene discussed is NR1H4; the disease is metabolic dysfunction-associated steatotic liver disease.