Although there is no precise understanding of the entire hypothalamic disorder, PWS mice models including Magel2 and Snord116 gene–inactivated mice (22-25) showed abnormal oxytocin-secreting neurons, development and function, and a defect of hormone maturation via decreased levels of Proconvertase 1 enzyme in the hypothalamus, pancreas, and stomach, explaining various levels of deficits of matured hormones (26). The gene discussed is OXT; the disease is Prader-Willi syndrome.