The TKI-resistance uncovered by this study differs from previously described mechanisms as it protects CML cells under conditions when the BCR-ABL kinase activity is inhibited and when the pro-survival pathways are also inhibited, that is, when the anti-apoptotic BCL2-proteins are reduced and the pro-apoptotic BIM protein is increased. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.