Some studies have shown that hepatic cholesterol synthesis is up-regulated in NAFL and NASH patients due to increased activity of a major regulator of cholesterol synthesis, sterol regulatory element–binding protein 2 and its downstream effector HMG CoA-reductase, which catalyzes a rate-limiting step in cholesterol synthesis [80–82]. This evidence concerns the gene HMGCR and metabolic dysfunction-associated steatohepatitis.