By addressing the epigenetic modifications that contribute to FTO overexpression and other genes involved in adipogenesis (RNA methyltransferase complex methyltransferase-like protein (METTL3), YTH domain-containing reader proteins (YTHDF1 or YTHDF3) together with the downstream effectors, it may be possible to mitigate some of the adverse metabolic and inflammatory outcomes associated with obesity [24,25]. Here, YTHDF1 is linked to obesity due to melanocortin 4 receptor deficiency.