11-Hydroxysteroid dehydrogenase type 2 (11-HSD2) plays a critical role in normal physiology in the corticosteroid regulation of sodium homeostasis and the pathophysiology of hypertension by converting active cortisol to inactive cortisone. Mutation in the gene encoding 11-HSD2 results in cortisol induction of hypertension and hypokalemia, a syndrome of apparent mineralocorticoid excess.1 Expression of 11-HSD2 mRNA and protein has been shown in placenta and mineralocorticoid target tissues, particularly the kidney.2 In mouse, expression of this enzyme is tissue- and developmentally specific, indicating the importance of the enzyme in regulating glucocorticoid-mediated maturation.3 Caymans 11-HSD2 polyclonal antibody detects a band at around 44 kDa in tissues such as kidney and cell lines including Caco-2 cells and HT-29 cells.