Non-obese NAFLD usually has higher TG levels when compared with matched controls.6 Our study focused on the non-obese NAFLD, and found that KAL was significantly elevated in HTG subjects and NAFLD patients and positively correlated with TG; Additionally, feeding with HFruD is the classical animal model of HTG, and KAL deficiency could significantly reverse the hepatic steatosis of HFruD rats; FFA, the consequent product of lipid metabolic dysfunction, cooperated with T3 and up-regulated KAL in hepatocytes. This evidence concerns the gene SERPINA4 and metabolic dysfunction-associated steatotic liver disease.