With respect to psychosis, it is highly probable that KP dysregulation could originate from neuronal and/or peripheral immune-dependent aberrations that could result to disturbed glutamatergic neurotransmission48,49, and consequently to the presentation of positive, negative, and cognitive symptoms as imposed by the long-lasting glutamate hypothesis of schizophrenia45,50. The gene discussed is NPPA; the disease is psychotic disorder.