Overall, these data suggested that although Mettl3 knockout suppressed glycolysis and thermogenesis in iWAT, different than the previous reported BAT‐specific Mettl3 knockout mice,[24] Mettl3 FKO mice were resistant to obesity under energy challenge, at least partially due to reduced proliferation of preadipocytes in iWAT by glycolytic product lactate mediated crosstalk between mature adipocytes and preadipocytes. The gene discussed is METTL3; the disease is obesity disorder.