Patients with PWS have dysregulation at the level of the hypothalamus of the orexigenic neuropeptide Y (NPY), agouti-related protein (AgRP), and gamma-aminobutyric acid (GABA) neurons as a consequence of the deletion of SNORD116 in the PWS critical region [5,6]. The gene discussed is NPY; the disease is Prader-Willi syndrome.