When the uptake of FFAs via FFA transporters, such as CD36, or de novo lipogenesis (DNL) in hepatic cells exceeds the export of FFAs via very-low-density lipoprotein (VLDL) packaging or the usage of FFAs by mitochondrial β-oxidation, hepatocellular fat gradually accumulates, which leads to NAFLD. This evidence concerns the gene CD36 and metabolic dysfunction-associated steatotic liver disease.