Meanwhile, an increasing number of studies in mouse models of Angelman syndrome demonstrate that Ube3a must be reinstated in late embryonic and early postnatal development to correct most neurological phenotypes (Silva-Santos et al., 2015; Gu et al., 2019; Rotaru et al., 2018; Sonzogni et al., 2020). The gene discussed is UBE3A; the disease is Angelman syndrome.