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]. The gene discussed is ATG7; the disease is metabolic dysfunction-associated steatotic liver disease.