USP7 is also mutated in a subset of children with similar phenotypes to those seen in PWS and SYS, providing further evidence that MAGEL2, with its binding partners, regulates biological pathways that are affected in patients with PWS and SYS.[14,15] There is consensus among researchers about the abundant expression of MAGEL2 in the hypothalamus. This evidence concerns the gene USP7 and Prader-Willi syndrome.