These findings, together with previous research in rodents and two prior studies in humans, provide preliminary support for the hypothesis that altered expression of the glucocorticoid receptor due to cytosine methylation of the gene promoter could be a mechanism of the neuroendocrine effects of early-life stress, and could predispose to the development of major depression and post-traumatic stress disorder. The gene discussed is NR3C1; the disease is major depressive disorder.