Several lines of experimental evidence supporting the role of UCP3 in EH came from human studies [see 6 and references within] and from mice over-expressing UCP3, being: (i) obesity-resistant mice present higher UCP3 levels than obesity-prone mice [15]; (ii) transgenic mice that over-express UCP3 are metabolically less efficient than their wild-type litter mates, and are protected against high fat diet (HFD)-induced obesity [16,17]; and, (iii) modest UCP3 over-expression in SkM increased mice energy expenditure [18]. The gene discussed is UCP3; the disease is Obesity.