Observational studies have extensively documented immune and metabolic dysfunctions in schizophrenia (1, 2), an archetypal psychotic disorder characterised by difficulties with, primarily, perception (e.g., hallucinations, delusions) and cognition (e.g., poor attention, memory). With lifetime prevalence of about 1%, schizophrenia typically manifests during second and third decades of life, has a chronic relapsing remitting course, and is thought to be linked with altered neurodevelopment (3). Pathophysiologic explanation and drug treatment for the illness is predicated on dopaminergic over activity in the mesolimbic pathway and underactivity is mesocortical pathway, but this is far from the full picture (4). Dopamine over activity is not present in all patients with schizophrenia, and about a third of patients do not respond to anti-dopamine antipsychotic drugs currently used to treat this illness (5), suggesting that other mechanisms are involved.