When the pathway reporters were transfected into those cells and treated with various concentrations of MBZ, we found that 11 of the 12 pathways, especially ELK/SRF, NFKB, MYC/MAX, E2F/DP1, TGF/SMAD and AP1 pathway reporters, were effectively inhibited by MBZ in a dose-dependent fashion although the CREB pathway reporter was seemingly activated by MBZ, suggesting that MBZ may exert its anticancer and anti-chemoresistance activities in ovarian cancer cells by inhibiting multiple cancer-related cell proliferation pathways in cisplatin-resistant ovarian cancer cells. The gene discussed is MAX; the disease is ovarian cancer.