In contrast to normal endometrium, the expression of aromatase is aberrant in endometriosis and is stimulated by prostaglandin E2 (PGE2). This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis--deficient 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) type 2 expression--impairs the inactivation of estradiol (E2) to estrone (E1). These molecular aberrations collectively favor accumulation of increasing quantities of E2, and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis with an aromatase inhibitor.