Furthermore, a recent study using induced pluripotent stem cells derived from the PWS patients revealed up-regulation of maternally expressed genes in the imprinted DLK1-DIO3 locus on chromosome 14 due to deficiency of the paternal allele of IPW, a long noncoding RNA at the 15q11–q13 locus that acts as a regulator of the DLK1-DIO3 region, and this indicates that a subset of PWS phenotypes may arise from dysregulation of an imprinted locus distinct from the PWS critical region of 15q11–q13 [7]. This evidence concerns the gene SNHG14 and Prader-Willi syndrome.