Cilostazol may inhibit lipid de novo synthesis and gluconeogenesis by activating the dual regulation of the AMPK-ACC1/SCD1 pathway and AMPK-PGC1α-G6P/PEPCK pathway, reduce lipid synthesis and glucose production in the liver, and correct glucose and lipid metabolism disorders in NAFLD mice under a high-fat diet, thereby improving liver lipid accumulation. Here, PCK2 is linked to metabolic dysfunction-associated steatotic liver disease.