Recent discoveries of somatic mutations permit the recognition of sub-types of aldosterone-producing adenomas (APA) with different clinical presentations and pathology. Here we describe two women who presented in pregnancy, and one woman who presented post-menopause, with hyperaldosteronism. Their APAs harbored activating mutations of CTNNB1, encoding β-catenin in the Wnt cell-differentiation pathway, and expressed >100-fold higher levels of LHCGR and GNRHR, encoding gonadal receptors, than other APAs. The mutations stimulate Wnt activation and cause adrenocortical cells to de-differentiate towards their common gonad-adrenal precursor cell-type.