MAGEL2 and Prader-Willi syndrome: With the caveat that studies on peripheral tissues, fibroblasts and lymphoblasts, may not accurately reflect gene expression in the brain, our results indicate that SNURF/SNRPN and the centromeric genes MKRN3, NDN and MAGEL2 are unlikely to play a prime role in the causation of PWS-associated features, although it remains an open question whether their loss or non-functioning might contribute to the more marked phenotypic expression that is seen in typical PWS.