For example, in breast cancer tissue: (1) the “sulfatase pathway” and “aromatase pathway” are upregulated, thereby providing a steady stream of precursors for estrogen synthesis in the form of inactive steroid sulfates or androgens, respectively, and (2) the reductive 17-β-hydroxysteroid dehydrogenases (17β-HSDs), which convert estrone (E1) into the more potent estrogen, estradiol (E2), are favored over the oxidative 17β-HSDs which inactivate E2 (reviewed in [44]) (Fig. 4a). The gene discussed is CYP19A1; the disease is breast cancer.