These studies generally discuss possible mechanisms for the blunted HPA axis response, including elevated levels of CRH-binding protein, enhanced sensitivity to the negative feedback of glucocorticoids (i.e., a higher abundance of glucocorticoids receptors at central level), secondary adrenal atrophy, etc. However, the therapeutic potential of CRH (or other pituitary secretagogues) to relieve the suppressed HPA axis in ME/CFS has generally not been considered. The gene discussed is NR3C1; the disease is myalgic encephalomeyelitis/chronic fatigue syndrome.