Although mice with paternal inheritance of the Δ4.8 mutation expressed relatively similar levels of the Snrpn, Snord116, and Snord115 transcripts as mice with maternal inheritance of the Δ4.8 mutation (Figure 8A, b and d), different phenotypic effects of the Δ4.8 mutation were found depending on the origin of inheritance: paternal transmission of the Δ4.8 mutation caused PWS phenotypes showing postnatal lethality and growth retardation [6]; maternal inheritance of the Δ4.8 mutation is able to complement postnatal lethality and growth retardation phenotypes in the PWS mouse models. This evidence concerns the gene SNORD116 and Prader-Willi syndrome.