Genetic models consist of mutagenesis or knockout of various isolated genes that are thought to be involved in the pathology of both syndromic and non-syndromic ASD, such as FMR1 (Fragile X syndrome), NF1 (Neurofibromatosis type 1), TSC1 (Tuberous sclerosis), DHCR7 (Smith–Lemli–Opitz syndrome), MeCP2 (Rett syndrome), and of genes known to be associated to high risk of ASD, such as SHANK2, CNTNAP2, eIF4E, and transgenic mouse targeting Oxytocin, Vasopressin, Reelin, Dishevelled-1, Sert (serotonin transporter), MAOA (monoamine oxidase A), HOXA1, PTEN, and Neuroligins [221]. This evidence concerns the gene MAOA and fragile X syndrome.