Notably, the maternal Δ4.8 chromosome expressed low levels of the paternally expressed imprinted genes Snrpn (21%–35%), Snord116 (8%), Snord115 (10%), and Ndn (28%) (Figure 1 and 2), which were however sufficient to complement postnatal lethality and growth retardation phenotypes in the mouse models of PWS. This evidence concerns the gene SNORD116 and Prader-Willi syndrome.