A Shank3-deficient rat model was generated, which showed disabilities similar to those seen in the Phelan-McDermid syndrome and interestingly, the deficits of the mutant rat could be ameliorated by intracerebroventricular oxytocin administration, implying that exogenous oxytocin administration might have therapeutic potential in human patients [42] (see Table 1A, Phelan-McDermid syndrome model). This evidence concerns the gene OXT and Monosomy 22q13.