This may have been perhaps the result of a relative secondary adrenal insufficiency, which leads to an amplified adrenal cortisol response due to an upregulation of ACTH receptors, but this sounds unjustifiable since the lack of continuous stimulation of the adrenal cortices would cause atrophy, rendering them non-responsive to a low- (and even high) dose of cosyntropin stimulation in the long run. The gene discussed is MC2R; the disease is Adrenal insufficiency.