Biallelic expression of CYFIP1 and NIPA2 in cultured lymphoblasts and brain tissues analyzed suggests that they are unlikely to be major contributors to the pathogenesis of PWS, but haploinsufficiency may contribute to a more prominent behavioral phenotype seen in PWS and Angelman syndrome (AS) patients with class I deletions as compared to those with class II deletions. Here, NIPA2 is linked to Prader-Willi syndrome.