Studies have shown that estrogen can bind to the ERE region of HMGCR promoter to activate HMGCR expression and induce the increase of human serum total cholesterol and LDL (39), while after liver steatosis and inflammation, its ability to inactivate estrogen is reduced, and positive feedback activates HMGCR expression and promotes lipid deposition in the bile.CYP7A1 plays a pivotal role in converting cholesterol into bile acids, serving as one of the liver’s primary mechanisms for cholesterol clearance (40). The gene discussed is HMGCR; the disease is fatty liver disease.