For instance, loss of function of the maternally-inherited ubiquitin protein ligase E3A (UBE3A) contributes to the onset of Angelman syndrome, while the loss of paternally expressed genes including small nuclear ribonucleoprotein polypeptide N (SNRPN) contributes to the onset of Prader-Willi syndrome13–15. This evidence concerns the gene UBE3A and Angelman syndrome.