Extensive dysregulation of hepatic cholesterol homeostasis has been documented in NAFLD, leading to increased hepatic cholesterol levels, which occurs at multiple levels, including the increased hydrolysis of cholesterol esters into free cholesterol (FC), increased hepatic cholesterol synthesis, increased levels of active SREBP2, increased uptake of cholesterol-rich lipoproteins, and decreased cholesterol excretion in bile [100,101,102,103,104]. The gene discussed is SREBF2; the disease is metabolic dysfunction-associated steatotic liver disease.