Since mice with congenital Snord116 deletions do not undergo the phenotypic transition seen in human PWS, we generated adult-onset Snord116 deletions to determine whether phenotypes mirroring later stages of human PWS (i.e., obesity and hyperphagia) might appear in the absence of a developmental growth phenotype. This evidence concerns the gene SNORD116 and obesity due to melanocortin 4 receptor deficiency.