The enzyme 11β‐hydroxysteroid dehydrogenase (11β‐HSD) catalyzes the interconversion between hormonally active cortisol and inactive cortisone within cells. There are two isozymes: 11β‐HSD1 activates cortisol from cortisone and 11β‐HSD2 inactivates cortisol to cortisone. 11β‐HSD1 was recently discovered in skin, and we subsequently found that the enzyme negatively regulates keratinocyte proliferation. We verified 11β‐HSD1 and 11β‐HSD2 expression in benign and malignant skin tumors and investigated the role of 11β‐HSD in skin tumor pathogenesis. Randomly selected formalin‐fixed sections of skin lesions of seborrheic keratosis (SK), squamous cell carcinoma (SCC), and basal cell carcinoma (BCC) were stained with 11β‐HSD1 and 11β‐HSD2 antibodies, and 11β‐HSD expression was also evaluated in murine epidermis in which hyperproliferation was induced by 12‐O‐tetradecanoylphorbol‐13 acetate (TPA). We observed that 11β‐HSD1 expression was decreased in all SK, SCC, and BCC lesions compared with unaffected skin. Conversely, 11β‐HSD2 expression was increased in SK and BCC but not in SCC. Overexpression of 11β‐HSD2 in keratinocytes increased cell proliferation. In the murine model, 11β‐HSD1 expression was decreased in TPA‐treated hyperproliferative skin. Our findings suggest that 11β‐HSD1 expression is decreased in keratinocyte proliferative conditions, and 11β‐HSD2 expression is increased in basal cell proliferating conditions, such as BCC and SK. Assessing 11β‐HSD1 and 11β‐HSD2 expression could be a useful tool for diagnosing and characterizing skin tumors.