When tested in vitro , 7-keto appears to activate the beta subset of the estrogen receptor (ERβ) with an EC 50 around 500μM which is partially blocked by exemestane (aromatase inhibitor or AI); there was no apparent activity on the classical subset (ERα) and parent DHEA and DHEAS were eqipotent.  As activity was hindered with an AI and there was efficacy in HepG2 cells but not Hep293 (expressing  and not expressing  aromatase, respectively) it is though that 7-oxo can be metabolized into an estrogen. 
In 2 unrelated patients, Ulick et al. (1979) described a disorder in the peripheral metabolism of cortisol, manifested by hypertension, hypokalemia, low plasma renin activity, and responsiveness to spironolactone. Aldosterone levels were subnormal. Although the features suggested primary mineralocorticoid excess, no overproduction of mineralocorticoid could be demonstrated. One of the patients, who had been reported by New et al. (1977), was a 3-year-old Zuni Indian girl with hypertension, hypokalemia, and decreased secretion of all known sodium-retaining corticosteroids. The second patient was a boy of Middle Eastern parentage who had a stroke with residual left hemiparesis at age 7, and was first found to be hypertensive at age 9 (blood pressure as high as 250/180 mm Hg). Other findings included growth retardation, grade III retinopathy, hypokalemia, and hyposthenuria. Biochemical studies indicated a decreased rate of conversion of active cortisol to cortisone, and the authors postulated a defect in 11-beta-hydroxy oxidation of cortisol. Ulick et al. (1979) suggested the term 'apparent mineralocorticoid excess.'