In a small percentage of Prader–Willi syndrome (PWS) patients who retain both parental copies of 15q11-q13, imprinting defects and promoter methylation have been identified, resulting from microdeletions targeted at the small nuclear ribonucleoprotein polypeptide N (SNRPN) gene [81,82,83]. This evidence concerns the gene SNRPN and Prader-Willi syndrome.