To verify whether METTL16-mediated m6A modification indispensably contributed to the overexpression of CIDEA in NAFLD, METTL16 transfection and gene silencing with METTL16 siRNA were performed in HepG2 cells to construct the overexpression and konckdown models of METTL16. The gene discussed is METTL16; the disease is metabolic dysfunction-associated steatotic liver disease.