Cortisol is a glucocorticoid that can bind the glucocorticoid receptor. The molecule of cortisol is similar to aldosterone that can bind the mineralcorticoid receptor. 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. Polycystic ovary syndrome (PCOS) is also believed to relate to the deficiency of cortisone conversion to cortisol. In human, there are two HSD-11β isoforms, including type 1 11β-HSD (11β-HSD1, NADPH-dependent) and type 2 11β-HSD (11β-HSD2, NAD + -dependent). It has been reported that 11β-HSD1 has bidirectional activity, while 11β-HSD2 mainly converts cortisol into cortisone. 11β-HSD1 is highly expressed in key metabolic tissues, including liver, adipose tissue, and the central nervous system. 11β-HSD2 is expressed in aldosterone-selective tissues, including kidneys, liver, lungs, colon, salivary glands, HSD2 neurons and placenta. HSD 11β play crucial roles in blood pressure regulation and yndrome of apparent mineralocorticoid excess.