POMC and adrenal gland hyperfunction: Whereas silent CAs are immunopositive for adrenocorticotropic hormone (ACTH), but do not manifest biochemical or clinical hypercortisolism5, the majority of clinically active CAs secrete excessive amounts of ACTH, causing chronic hypercortisolism due to lack of hypothalamus–pituitary–adrenal (HPA) axis feedback regulation at the level of the CA, leading to manifestations of the clinical features of Cushing’s disease1.