Beyond the UCP1 KO model, the control of obesity resistance by adipose FGF21 may also explain the lack of obesity resistance in other important BAT-deficient mouse models, such as mice lacking ß-adrenergic receptors (ß-less) or mice with isolated BAT deficiency (UCP1-DTA)6,7. Here, UCP1 is linked to obesity due to melanocortin 4 receptor deficiency.