Individuals with PWS have dysregulation at the level of the hypothalamus of Neuropeptide Y (NPY), agouti related protein (AgRP), and gamma-aminobutyric acid (GABA) neurons, which appear to be associated with the deletion of SNORD116 in the PWS critical region resulting in hyperphagia [1,3]. The gene discussed is NPY; the disease is Prader-Willi syndrome.