Recently, our group described the existence of a milder form of AME (nonclassic AME or NC-AME), characterized by an increased serum cortisol to cortisone ratio and low serum cortisone associated with normal-elevated systolic blood pressure (BP), and MR activation (detected by lower renin and a higher urinary potassium excretion rate) [4], suggesting the existence of a distinctive phenotypical spectrum in these subjects, which may be prevalent in a primary care cohort. The gene discussed is NR3C2; the disease is apparent mineralocorticoid excess.