These results are in line with the view of UBE3A as a ‘molecular tightrope’ in neurons [43], as suggested by the several mechanisms in place to continually adjust neuronal UBE3A activity (genetic imprinting, stimulation by cancer-causing E6 virus [44], phosphorylation via PKA [45]) and the range of different neurodevelopmental disorders due to aberrant levels or functioning of UBE3A (AS, autism, epilepsy, intellectual disabilities). This evidence concerns the gene UBE3A and cancer.