This severely complicates investigation because it means that for every observation of a relationship between energy intake, leptin/insulin and dopamine we have to ask “does this observation reflect normal function or pathological adaptation?” This situation increases the risk of making inappropriate inferences of normal function from pathological conditions and vice-versa, an issue addressed below (cage-induced obesity section). The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.