The endogenous OT systems are believed to be involved in the pathogenesis of ASD, based on results indicating low levels of plasma OT [34], alterations in OT peptide forms [35], sexually dimorphic patterns of OT associated with anxiety [36], dysregulation of OT signaling pathways [37] and common polymorphisms of the CD38 gene (CD38) [38,39,40,41] and OT receptor genes (OTR) [42,43] in individuals with ASD. This evidence concerns the gene CD38 and Anxiety.