The pathological mechanism of NAFLD is excessive lipid accumulation in the liver due to imbalanced fatty acid synthesis and oxidation [32], which are orchestrated by the interaction of multiple factors, including SREBP-1, an important transcriptional modulator involved in hepatic lipid metabolism that is involved in transcriptional regulation of lipogenic enzymes (FAS and ACC), regulation of fatty acid biosynthesis and VLDL assembly, and intracellular fatty acid trafficking [27, 33]. This evidence concerns the gene FAS and metabolic dysfunction-associated steatotic liver disease.