Studies have shown that the hepatic expression of SREBP-1c and its target lipid synthesis regulation genes, FAS and ACC, increase several times both in patients with NAFLD and in animal models such as transgenic mice, ob/ob mice (leptin deficiency results in an insulin resistance and hyperinsulinemia), and high-fat diet-fed mice and rats, which leads to deposition of a large amount of TG [16–20]. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatotic liver disease.