Our results support the involvement of the immune-activated KP of TRP metabolism in the pathophysiology of a subset of people with schizophrenia having elevated cytokines from five distinct aspects: (1) elevation of KP enzyme mRNAs in human brain, (2) alterations of KP metabolites in human brain, (3) peripheral changes in KP metabolites, (4) peripheral KP measures that link with cognitive deficits, and (5) peripheral KP measures that link with structural human brain volumetric abnormalities. The gene discussed is NPPA; the disease is Cognitive impairment.