Contributing factors likely include the downregulation of corticotropin-releasing hormone (CRH) and proopiomelanocortin (POMC) —the prohormone to ACTH— and corticotroph atrophy due to chronic suppression of the HPA axis and the upregulation of cytokines and prostaglandins following treatment of hypercortisolism. The gene discussed is CRH; the disease is adrenal gland hyperfunction.