In the recent years, SNORD116 has emerged as a critical, and possibly, determinant candidate in PWS not only by its highly conserved sequence in the minimal critical region, but also because paternal deletions affecting the expression of NDN, MKRN3, MAGEL2, or SNORD115 genes do not address the full spectrum of PWS symptoms (10, 100, 123, 135, 136). This evidence concerns the gene SNORD116 and Prader-Willi syndrome.