Although imatinib (IM) was first developed as an inhibitor of BCR-ABL kinase for treatment of CML, the development of drug resistance became obstacle of its success in clinic, which was attributed to not only BCR-ABL gene amplification and kinase domain mutation, but also low oral bioavailability, high plasma-protein binding efficiency and altered drug efflux and/or influx mechanisms (Apperley, 2007; Milojkovic and Apperley, 2009). This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.