CRF induces the release of adrenocorticotropic hormone (ACTH), where it stimulates the synthesis and secretion of glucocorticoids, with cortisol as the end product.6 Furthermore it has been observed that augmented HPA-axis responses towards challenges in normotensive individuals enhance the risk of developing hypertension.8 Dysregulation of the HPA axis may also be a result of unmitigated increases in cortisol where prolonged elevations ultimately result in the down-regulation of CRF, ACTH and subsequently cortisol.9 The gene discussed is POMC; the disease is hypertensive disorder.