SummaryIn most aldosterone-producing adenomas (APA) dedifferentiation occurs with formation of transitional cells, bearing characteristics of both glomerulosa and fasciculata cells. These cells are able to produce Cortisol, and their aldosterone production follows the circadian rhythm of ACTH. Usually, no clinical signs of Cortisol excess develop, since the Cortisol production remains under ACTH feedback control. Only a few cases have been described with autonomous Cortisol secretion, not suppressible by low dose dexame-thasone. We present a patient with an APA, synthesizing enough Cortisol to cause the typical clinical expression of Cushing’s syndrome. Possible etiopathological mechanisms are discussed.