These models were characterized by a pronounced overrepresentation of gene expression changes typically observed during postnatal development and included serotonin transporter knockout mice, glucocorticoid receptor overexpressing mice, and corticosterone-treated mice, models of depression and anxiety, Df(16)A<sup>+/-</sup> mice, a 22q11.2 deletion schizophrenia model, β-glucuronidase-deficient lysosomal storage disorder model mice, and senescence-prone SAMP8 mice. This evidence concerns the gene NR3C1 and schizophrenia.