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Full list of author information is available at the end of the articleChronic myeloid leukemia (CML) is a hematopoietic dis-order characterized by unregulated proliferation of predom-inantly myeloid cells in the bone marrow [1]. BCR-ABL fusion proteins resulting from the chromosomal transloca-tion t(9;22) (the Philadelphia chromosome: Ph) cause CML [2]. BCR-ABL activity leads to uncontrolled cell prolifera-tion, reduced apoptosis, and malignant expansion of hematopoietic stem cell populations. The ABL tyrosine kin-ase inhibitor (TKI) imatinib has dramatically improved the However, some patients, particularly those with advanced-phase CML, have developed resistance to imatinib [4]. More than 50 distinct point mutations in the kinase do-main of BCR-ABL have been detected in patients with imatinib-resistant CML; point mutations in this domain are the most frequent cause of acquired imatinib resistance in CML patients [5,6]. Second-generation TKIs, such as dasatinib and nilotinib, have shown promising results in imatinib-resistant CML patients, but dasatinib and nilotinib are not effective against CML clones with T315I mutations [7]. Recently, ponatinib (also known as AP24534) was iden-tified as a potent oral tyrosine kinase inhibitor and wa