Targeted deletion of the PPAR-γ in hepatic tissue could significantly reduce NAFLD pathogenesis in HFD-fed mice by downregulating the expressions of FA transporters (CD36, liver-type FA-binding protein, and MTP) and DNL promoters (stearoyl-CoA desaturase 1, SREBP-1, and ACC). Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.