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). This evidence concerns the gene SMARCA4 and Prader-Willi syndrome.