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Since mineralocorticoid shares much similarity with glucocorticoid, HSD-11β oxidizes cortisol to inactive cortisones to prevent the illicit activation of mineralocorticoid or glucocorticoid receptors in different tissues. HSD-11β co-localizes with intracellular adrenal steroid receptors. Deficiency of HSD-11β will cause severe conditions known as apparent mineralocorticoid excess syndrome (AME), which is characterized as low potassium level, hypertension and reduced plasma renin.