Increased levels of endogenous NMDAR antagonists, N-acetylaspartyl-glutamate and kynurenic acid [85,86,87], and/or the decreased activity of glutamate carboxypeptidase II in schizophrenia may support the hypothesis that N-acetylaspartyl-glutamate signaling is involved in NMDAR hypofunction in schizophrenia [79,80,81,82,83,84]. This evidence concerns the gene FOLH1 and schizophrenia.