Over the past decades, several research groups have formulated a hypothesis relating alterations in cortisol, corticotrophin (ACTH), and corticotrophin-releasing hormone (CRH) functions to the causality of depression and proposed that antidepressants may act through normalization of the hypothalamus-pituitary-adrenal axis (HPA) dysfunctions [46]. This evidence concerns the gene CRH and depressive symptom measurement.