Further studies found that the overexpression of Mettl14 and Mettl3 promotes fatty acid synthesis and lipid accumulation by stabilizing the mRNAs of ATP citrate lyase (Acly) and stearoyl-CoA desaturase 1 (Scd1) and accelerating NAFLD to HCC127, while adipose tissue Mettl3 and Mettl14 modify Adrb2/3, adipose triglyceride lipase (Atgl), and comparative gene identification 58 (Cgi58) transcripts to impair β-adrenergic signaling, reducing lipolysis and worsening obesity/NAFLD128. The gene discussed is METTL14; the disease is obesity due to melanocortin 4 receptor deficiency.