The findings of this work raise the intriguing possibility that aberrant upregulation of adipose Mettl3, Mettl14, and m6A methylation of Adrb2, Adrb3, Atgl, and Cgi‐58 transcripts, and translational suppression of these transcripts may explain adipose catecholamine resistance and lipolysis suppression in obesity. Here, METTL14 is linked to obesity due to melanocortin 4 receptor deficiency.