Mice in which specific genes associated with the PWS syndrome have been knocked out similarly develop late-onset obesity due to hyperphagia, and this can be partly explained by a deficient production of oxytocin in the hypothalamus (Dombret et al., 2012) or by a reduction in the number of oxytocin neurons (Muscatelli et al., 2000). Here, OXT is linked to obesity due to melanocortin 4 receptor deficiency.