DRD2 and 22q11.2 deletion syndrome: This mechanism integrates several competing schizophrenia theories, such as dopamine hyperactivity or hyperfunction hypothesis (Carlsson, 1988) (because the Drd2 expression level is abnormally elevated in the thalamus of 22q11DS mice), glutamatergic hypofunction hypothesis (Coyle, 1996, 2006) (because disruption occurs at glutamatergic thalamocortical synapses), thalamocortical dysconnectivity hypothesis (Friston and Frith, 1995; Woodward et al., 2012), and thalamocortical loop dysfunction hypothesis (Behrendt, 2003).