Integrating these different streams of evidence, we assumed that the common schizophrenia-associated intronic variants of GRIN2A lead to reduced expression of the NR2A subunit, which should particularly affect Parvalbumin-positive interneurons and thus cause a disinhibition of glutamatergic pyramidal cells (Fig. 1d) as suggested both by pharmacological models of schizophrenia and the phenotype of exonic GRIN2A loss of function variants. This evidence concerns the gene PVALB and schizophrenia.