Although the molecular mechanism leading to the development of hepatic steatosis in the pathogenesis of nonalcoholic fatty liver disease is complex, animal models have shown that modulating important enzymes, such as ACC, FAS, and SCD-1, in fatty acid synthesis in liver may be a key for the treatment of nonalcoholic fatty liver disease [19]. This evidence concerns the gene FAS and metabolic dysfunction-associated steatotic liver disease.