In NAFLD, the excess of triglycerides and FFAs suppresses the initiation of autophagy through activation of mammalian target of rapamycin (mTOR) and the suppression of serine/threonine-protein kinase ULK1 activity, leading to increased hepatic oxidative stress (57, 58). This evidence concerns the gene ULK1 and metabolic dysfunction-associated steatotic liver disease.