In addition, we predict that complex gene variants as well as unique gene mutations present in major and minor traits of disease may lead to the onset of the full-complex disorders.85 We postulate that the SCZ–T2D association may mask common pathological pathways, and that either the impaired dopamine and/or PRL pathway in SCZ may impair glucose homeostasis, thereby contributing to T2D. Here, PRL is linked to type 2 diabetes mellitus.