The most plausible mechanism by which androgen excess stimulates growth of ER-positive/AR-positive cancers is increased conversion to estrogens, as suggested by the well-documented finding of estradiol concentrations 10 times higher in tumor tissue than in blood [20-27] and by evidence of increased expression of estrogen-producing enzymes in breast cancer tissue [28-35], which is suggestive of local synthesis of estradiol from androgen precursors. The gene discussed is AR; the disease is breast carcinoma.