The D3R/dysbindin interaction has been shown to promote D2R/D3R imbalance by favoring an increase in D2R signaling in the PFC but not in the striatum [55], underlining the potential role of regional D2R/D3R reciprocal ratio of occupancy and D3R antagonism in improving cognitive symptoms in schizophrenia. Here, DTNBP1 is linked to schizophrenia.