MAGEL2 and Prader-Willi syndrome: In most cases (70%), the large deletion (LD) of paternal 15q11-q13 region, comprised of several expressed protein-coding genes (MAGEL2, SNURF, and SNRPN, among others), a cluster of C/D box small nucleolar RNA noncoding genes (including SNORD116 and SNORD115), and several long noncoding transcripts (including IPW and the antisense transcript to UBE3A), leads to PWS pathogenesis [1,2,3].