By the beginning of the 21st century, the HPA axis function was found to be often abnormal in patients with depression.[7–10] Under normal circumstances, activation of the HPA axis leads to the hypothalamus releasing corticotropin-releasing hormone (CRH), which in turn stimulates the pituitary to release adrenocorticotropic hormone (ACTH), ultimately leading to the synthesis and release of glucocorticoids such as cortisol (CS) and corticosterone (CORT). The gene discussed is CRH; the disease is depressive symptom measurement.