An additional syndromic autism linked with Ca2+ signaling dysregulation is Angelman Syndrome (AS), which is characterized by the deletion of the maternal allele of 15q13-11, including the gene UBE3A. In the UBE3A maternal allele null mouse model, disruptions in the autophosphorylation of CaMKIIα, which is essential for its kinase activity, is responsible for LTP deficits of the hippocampus [102]. This evidence concerns the gene UBE3A and Angelman syndrome.