Consistent with the NAFLD mouse model, SQLE overexpression also activated cholesterol and lipid biosynthesis in the human NAFLD cohort through the upregulation of hepatic sterol regulatory element-binding protein 1 (SREBF1), FASN, and SCD1 expression to drive the progression of NASH (Liu et al., 2021). The gene discussed is SCD; the disease is metabolic dysfunction-associated steatotic liver disease.