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. The gene discussed is CPT1A; the disease is metabolic dysfunction-associated steatotic liver disease.