These data clearly demonstrated that FM04 can overcome the unresponsiveness from the oral-dosed PTX in vivo because FM04 inhibited both active transporter P-gp in the GI tract (Figure 7A) and PTX metabolic CYP enzymes (Figure 7B–D) to boost the oral PTX bioavailability and eventually PTX achieved its plasma therapeutic level to kill the tumor cells. The gene discussed is PGP; the disease is neoplasm.