As TGZ induces PRODH/POX [27], and estrogens stimulate collagen biosynthesis [12,13,14,15] utilizing free proline and limiting its availability for PRODH/POX-dependent apoptosis, it has been considered that estrogen receptor status of breast cancer cells could determine ability of TGZ to induce PRODH/POX-dependent apoptosis. The gene discussed is PRODH; the disease is breast cancer.