Prader-Willi syndrome (PWS) is defined by simultaneously non-functioning genes on the paternal chromosome in the critical region 15q11.2–q13, which includes five small nucleolar RNA (SnoRNA), one of which is of interest to this thesis: SnoRNA116/HBII-85. The syndrome has a prevalence of 1:15,000 – 1: 30,000 and the complex physical, behavioural and intellectual difficulties are characterized through four phenotypic phases that correlate with age. Though these phases are individualized in timing and severity, all with PWS will experience phase three: hyperphagia (mean: - 8 years of age) and will need multiple, life-long intervention programs against the prediction of obesity.