Elevated AVP theoretically could increase hepatic glucose output via acting on the hypothalamic-pituitary-adrenal axis resulting in higher cortisol levels via V1b receptors [13]; we have previously proposed that high AVP caused from low fluid intake could elicit a Cushing’s syndrome-like phenotype due to the lack of negative feedback loop in AVP-mediated adrenocorticotropic hormone release [14]. Here, AVP is linked to Cushing syndrome due to macronodular adrenal hyperplasia.