As similar growth results have been reported in another ‘full’ genetic mouse model for PWS (Stefan et al. 2005, Ding et al. 2008), whereas mice with specific deletion of Magel2 exhibit normal skeletal growth (Bischof et al. 2007); this aspect of the PWS phenotype appears to be dependent upon lack of expression of one or more of the other genes within the PWS locus. Here, MAGEL2 is linked to Prader-Willi syndrome.