Moreover, genetic and pharmacological manipulation of the Golgi PtdIns4P–CUL7FBXW8–ATGL axis in mouse models of simple hepatic steatosis and MASH, as well as during ex vivo perfusion of a human steatotic liver graft leads to the amelioration of steatosis, suggesting that this pathway might be a promising target for metabolic dysfunction-associated steatotic liver disease and possibly MASH. This evidence concerns the gene PNPLA2 and fatty liver disease.