Consistent with their functions, we detected the upregulations of CD36, FAS, ACC, SCD1, SREBP-1c, and all pro-inflammatory cytokines, while the downregulations of PPARα and CPT1A in in vitro and in vivo NAFLD models, and demonstrated the potency of MEG3 in reversing these changes. Here, CD36 is linked to metabolic dysfunction-associated steatotic liver disease.