The favored strategy has not been the ectopic expression of UBE3A (Daily et al., 2011), amid fears of elevating the dosage of UBE3A, a known cause of the autism and epilepsy-related Dup15q syndrome (Lusk et al., 2021), but rather the reactivation of the intact, albeit silenced paternal copy of the UBE3A gene. This evidence concerns the gene UBE3A and autism.