Supporting a role for NAAG in the pathophysiology of schizophrenia, increased GCPII and reduced mGluR3 protein levels have been described in the dorsolateral prefrontal cortex of schizophrenia patients postmortem [126], and a disruption in NAAG-mediated signaling has been suggested in the postmortem schizophrenic anterior hippocampus [127]. The gene discussed is GRM3; the disease is schizophrenia.