This is observed in PORD, where females virilize in utero due to decreased CYP17A1 activity and reduced placental CYP19A1 activity, while CYP21A2 activity is also attenuated, depending on the POR mutation [90–92], suggesting increased steroid precursors for conversion in the adrenal backdoor pathway are produced and turnover of androgens into estrogens are reduced [90, 93, 94]. The gene discussed is CYP19A1; the disease is congenital adrenal hyperplasia due to cytochrome P450 oxidoreductase deficiency.