The current hypothesis of schizophrenia claims that the positive symptoms of the disease are linked to hyperactive dopaminergic activity, mediated by D2 dopamine receptors (D2R) in subcortical brain regions such as the striatum and the nucleus accumbens (Toda and Abi-Dargham, 2007; Lindenmayer et al., 2013), while the deficits in dopamine activity mediated by D1 dopamine receptors (D1R) are responsible for the negative symptoms and cognitive impairment (Toda and Abi-Dargham, 2007; Lindenmayer et al., 2013). This evidence concerns the gene DRD1 and schizophrenia.