Given the overlap in phenotypes between the N2KO, Snord116m+/p− mouse model, and PWS in humans, and the finding that Nhlh2 is downstream of Snord116, we sought to determine if deletion of Snord116 in the Snord116m+/p− mouse model affected the response to dietary CLA. This evidence concerns the gene NHLH2 and Prader-Willi syndrome.