The DA hypothesis of ASD is supported by alterations in the dopaminergic metabolism and transmission in several different mouse models such as Df(h22q11)/+ mice (model for the human 22q11.2 microdeletion syndrome) (41), Cntnap4 KO (KO model of a protein highly associated to ASD and schizophrenia) (42), Ube3a KO (model for Angelman syndrome) (43), Chd8+/− mice (model for the CHD8-related syndrome) (44), and VPA (model for the prenatal exposure to valproic acid) (45). The gene discussed is CNTNAP4; the disease is Angelman syndrome.