In the chimeric gene, acquisition of the adrenocorticotropic hormone (ACTH) responsive elements of CYP11B1, along with the CYP11B2 sequences encoding aldosterone synthase, explained both the ectopic expression of aldosterone synthase in the adrenocortical zona fasciculata, which normally secretes cortisol, and the correction of FH-1, i.e., resolution of the hyperaldosteronism and normalization of the high blood pressure (BP) values, with suppression of the ACTH-drive by glucocorticoid treatment. This evidence concerns the gene POMC and hyperaldosteronism.