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Several lines of evidence implicate glutamatergic dysfunction in the pathoaetiology of schizophrenia [1]. It is not clear, however, whether the degree of glutamatergic dysfunction is similar across individuals with schizophrenia or whether there is significant interindividual variability over and above the variability observed in the general population. Meta-analyses of 1H-MRS studies report higher glutamate and combined glutamate and glutamine (Glx) in the basal ganglia [2, 3], higher glutamine in the thalamus [2, 3] and lower glutamate in the medial frontal cortex (MFC)[3–6] in schizophrenia in comparison to controls. Two meta-analyses do not report lower glutamate levels in the medial frontal cortex [2, 3]