A reduction in GH signaling, through either GH deficiency or reduced GHR activity, leads to an upregulation of the fatty acid transporter Cd36, and several genes involved in lipogenesis (Fasn, Scd1) resulting in hepatic accumulation of triglycerides and lipid, leading to the development of nonalcoholic fatty liver disease (NAFLD; reviewed in Kaltenecker et al., 2018). This evidence concerns the gene FASN and metabolic dysfunction-associated steatotic liver disease.