Interestingly, a mouse model of schizophrenia induced by perinatal treatment with ketamine was reported to display a persistent reduction of glutathione and increased oxidative stress in the medial prefrontal cortex [87], which was accompanied by impaired mitochondrial function, reduced parvalbumin expression, and disruption of the excitation–inhibition balance (reduced inhibition onto layer 2/3 pyramidal cells, and increased excitatory drive onto parvalbumin-positive interneurons). This evidence concerns the gene PVALB and schizophrenia.