Studies have shown that in mice with HFD, the deletion of the Tfeb, ATG7, and ATG14 genes in hepatocytes, which encode vital autophagy regulators, as well as the deletion of the Atg5 gene in myeloid or endothelial cells, is associated with increased lipid accumulation in the liver and the development of NAFLD [121–123]. This evidence concerns the gene ATG5 and metabolic dysfunction-associated steatotic liver disease.