Moreover, the small molecule tyrosine kinase (TK) inhibitor imatinib (Glivec, Gleevec, STI571) used for the treatment of BCR-ABL-positive chronic myelogenous leukaemia or acute lymphoblastic leukaemia, despite being reported to be a substrate for ABCB1 and ABCG2 (with several reports stating that it is also transported by ABCC1), seems to increase the intracellular concentration of other ABC protein substrates in cancer cells: for example, combined with vincristine, enhanced vincristine sensitivity of MDR K562 cells (which overexpress ABCB1) in a human nude mice xenograft model. This evidence concerns the gene ABCG2 and chronic myelogenous leukemia, BCR-ABL1 positive.