We already know that aldosterone, by binding to mineralocorticoid receptors, activates different mechanistic pathways for anxiety and depression; a reduction of its levels as seen in post-adrenalectomy status improves the aldosterone exposure of central nervous system areas, while mineralocorticoid receptors antagonists for PA patients target receptors from different locations, and some exposure to cortisol becomes the main ligand in persons with Connshing syndrome [71]. This evidence concerns the gene NR3C2 and depressive symptom measurement.