Both AVP and OXT exert conserved function by mediating social behavior in mammalian species (Veenema and Neumann, 2008) and alterations in AVP and OXT in humans are associated with social dysfunction that is aggravated by ES: both are linked to social dysfunction in autism (Al-Ayadhi, 2005; Andari et al., 2010), schizophrenia (Goldman et al., 2008; Averbeck et al., 2012), depression (Heuser et al., 1998; Anderberg and Uvnäs-Moberg, 2000), and personality disorders (Coccaro et al., 1998; Lee et al., 2009). This evidence concerns the gene AVP and autism.