For instance, mice deficient in BAT or iWAT exhibit obese phenotypes under ambient temperature conditions.[27, 28, 29] In contrast, UCP1‐deficient mice do not develop obesity under the same conditions and only become obese when kept under thermoneutrality.[22, 30] This apparent contradiction in the metabolic phenotypes between these mouse models implies the existence of UCP1‐independent mechanisms through which brown and/or beige fat contribute to the regulation of whole‐body energy homeostasis. This evidence concerns the gene UCP1 and obesity due to melanocortin 4 receptor deficiency.