Since the identification of the minute Philadelphia chromosome in 1960 and its subsequent identification as a translocation with chromosome 9, our evolving understanding of the structure and function of the BCR-ABL1 aberrant tyrosine kinase has led to incredible advances in our understanding of the pathogenesis and treatment of CML. This understanding culminated in the development of IM, and this has been rapidly followed by second- and subsequent-generation agents that have built on the understanding of the action of IM and the development of resistance to it.

The complex of imatinib and other small-molecule ABL1 inhibitors as determined by analysis of crystal structures will continue to assist in the development and optimization of inhibitors that are active against mutations conferring resistance in CML (120). The rapidity with which these developments have been occurring is truly astounding and underlies the continued optimism that the treatment of CML and disorders related to it and other disorders where the molecular mechanisms of disease are being unraveled, will become more and more treatable in the future. There is little doubt that combination therapy of CML and related disorders will be a reality in the not-distant future (121).

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