Increased de novo FFA synthesis and uptake play crucial roles in the pathogenesis of hepatic lipid deposition and NAFLD.31 Increased expressions of FASn and CD36, the key enzymes that control FFA synthesis and uptake, respectively, played crucial roles in the development and progression of NAFLD in humans and animals,44,45 and hepatic CD36 disruption improved HFD-induced steatosis.46 In the present study, we observed that hepatic RIMKLA overexpression significantly decreased the protein expression of FASn and CD36 in ND, HFD, and db/db mice livers. Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.