“…As we previously highlighted (Gragnoli, Reeves, Reazer, & Postolache, ), the PRL‐pathway genes ( PRL , PRLHR , PRLR , OXT , OXTR , and NPY ) may thus contribute to SCZ, T2D, and/or MetS. Several studies suggest that the PRL‐pathway may contribute to SCZ‐mental traits: (a) male‐PRL levels are reduced compared to female‐PRL levels, and SCZ has earlier onset in males (Hafner, Maurer, Loffler, & Riecher‐Rossler, ); (b) PRL levels have been reported decreased (Meaney & O'Keane, ; Rao et al, ) as well as increased in SCZ drug‐naive patients (Gonzalez‐Blanco et al, ), and decreased in depression (Depue et al, ); (c) PRL increases with anti‐depressant (Faron‐Gorecka et al, ) and typical anti‐psychotic action (Oberweis & Gragnoli, ); (d) a more severe SCZ first‐episode is associated with decreased PRL (Gorobets & Matrosova, ); (e) PRL is an anxiolytic secreted during stress response (Insana & Wilson, ; Torner et al, ) and enhances bonding, social interaction, and attachment (Gordon et al, ; Neumann, ); and (f) PRL‐levels changes are associated with dissociative symptoms of depression (Bob et al, ). Thus, PRL‐levels changes are associated with SCZ; however, association does not imply causality.…”