Several independent cohort studies have shown that ∼60% of PWS individuals with the matUPD genotype develop psychotic symptoms in adulthood, and thus, it has been theorized that an imbalance in genomic imprinting via increased dosage of UBE3A may predispose PWS matUPD individuals for development of psychosis (Vogels et al., 2004; Soni et al., 2007; Sinnema et al., 2011; Crespi et al., 2018). This evidence concerns the gene UBE3A and Prader-Willi syndrome.