An increase in the consumption of dietary cholesterol represents the main root to complications in the nonalcoholic fatty liver disease (NAFLD), such as nonalcoholic steatohepatitis (NASH) [1, 2]; in fact, interference in cholesterol synthesis has proved to induce protective effects against ischemia-reperfusion injury; in addition, cholesterol overload in hepatocytes sensitizes to damage mediated by death receptors ligands such as TNF-α and FAS [2]. This evidence concerns the gene FAS and metabolic dysfunction-associated steatotic liver disease.