While the loss of the Snord116 locus was first hypothesized 10 years ago to be responsible for the pathogenesis of PWS (29), research has focused on the roles of the orphan snoRNAs, SNORD116 and SNORD115, and editing of the serotonin receptor (5htrc) by SNORD115 (14). The gene discussed is SNORD116; the disease is Prader-Willi syndrome.