Additional studies have also suggested that UBE3A may play a role in transcriptional regulation.127 Consequently, loss-of-function mutations within the maternal allele of UBE3A lead to intellectual disability, seizures, developmental delays and other comorbidities.128 Despite a decade of research performed with animal models, the pathophysiological mechanisms linking dysfunction of the UBE3A maternal allele to the AS neurodevelopmental phenotype remain poorly understood. Here, UBE3A is linked to Global developmental delay.