These results raise a possibility that gene(s) other than Snord116, and Snord115, and Snrpn are also involved in these PWS phenotypes, although deficiency of SNORD116 in human or Snord116 in mice has been demonstrated to contribute to PWS pathogenesis [9], [10], [11], [12], [13]. This evidence concerns the gene SNRPN and Prader-Willi syndrome.