Somatic mutations in SMARCA4, EPHA3, KRas, NRas, MAP2K1, and PDGFR-β have also been identified in PWS (165, 174) and they may act as “second hit” mutations for germline mutations such as RASA1, to create the PWS phenotype (165). The gene discussed is NRAS; the disease is Prader-Willi syndrome.