Less commonly, the aforementioned 11β-and 3β-hydroxylase deficiency, fetal androgen production in a bisexual gonad (ovotestis) or androgen-producing Tumor, maternal androgen production (tumor, luteoma), maternal androgen intake (progesterone, danazol) or deficiency of fetoplacental aromatase may lead to fetoplacental hyperandrogenemia. The gene discussed is CYP19A1; the disease is neoplasm.