Studies have shown that, as a regulator of hepatic lipid regeneration, LXRα is involved in the pathogenesis of hepatic steatosis in patients with MASLD (4), and when LXRα overexpression activates the important regulator of adipogenesis, sterol regulatory element binding protein 1c (SREBP-1c), and fatty acid synthase, which controls fatty acid synthesis (fatty acid synthase, FAS), which controls fatty acid synthesis, a large amount of fatty acid streams pool in the liver, thereby inducing MASLD (5). Here, FAS is linked to metabolic dysfunction-associated steatotic liver disease.