More recently, an antiproliferative action of estrogen was suggested to occur via activation of the epithelial ERβ.[13–15] The aromatase knock-out (ArKO) mouse is estrogen deficient and develops prostatic hyperplasia and hypertrophy,[16] both of which are suppressed and/or ablated in intact animals following the administration of an ERβ-specific (but not ERa) agonist.[17]. The gene discussed is CYP19A1; the disease is benign prostatic hyperplasia.