Loss of imprinted genes at the PWS-chromosome domain, such as the Magel2, Snord116, and Ndn genes in mice, caused behavioral and neuroendocrine alterations reminiscent of PWS (Muscatelli et al, 2000; Bischof et al, 2007; Kozlov et al, 2007; Qi et al, 2016; Burnett et al, 2017). This evidence concerns the gene NDN and Prader-Willi syndrome.