Critically, the selective deficits observed in our study are precisely in line with our expectations given (i) the broad NOS1AP expression pattern, (ii) the reported NOS1AP overexpression in other brain regions described in patients with schizophrenia [4,5] and depression [6], (iii) the differential contribution of the hippocampus along its longitudinal axis (e.g. reviewed in [44]) (iv) the high variability of symptoms in patients, and (v) the vast number of other molecules/pathways associated with mental disorders [39]. Here, NOS1AP is linked to depressive disorder.