In ME/CFS and FM, several potential mechanisms have been described as underlying hypercortisolism or hypocortisolism, characterized by high or low levels of circulating cortisol (corticosteroids), respectively, which involve the release of neurohormones, corticotropin-releasing hormone (CRH), and arginine vasopressin (AVP) from the hypothalamus, stimulating their receptors and leading to the release of adrenocorticotropic hormone (ACTH) from the pituitary into systemic circulation, affecting the release of glucocorticoids from the adrenal cortex [45,72,73]. The gene discussed is POMC; the disease is adrenocortical insufficiency.