HMGCS2 and metabolic dysfunction-associated steatotic liver disease: A recent report using liver- and kidney-specific gene knockout of Hmgcs2 indicates that renal HMGCS2 overexpression observed in kidney upon fasting does not contribute to whole body ketogenesis [38], while the contribution of hepatic HMGCS2 is essential to avoid the development of non-alcoholic fatty liver disease [39], as HMGCS2 would diminish the lipid load in the liver by redirecting lipids into ketone bodies synthesis.