There may be no better example of innovation in the field of leukemia and lymphoma therapeutics than the development of Abelson (Abl) kinase inhibitors for the treatment of chronic myeloid leukemia (CML). The year 2008 will mark a decade since CML patients were first treated with CGP57148 (STI571) now know as imatinib (Gleevec™, Novartis Pharmaceuticals, East Hanover, New Jersey, U.S.; Glivec®, rest of the world). While it is certainly not the first anticancer therapy directed at a known molecular target, the development of Abl kinase inhibitor “targeted therapy” for CML has set a clear example of the proof of principle in validating molecular targets and a high bar of success to which other innovative therapies are compared. The natural history of CML has been irrevocably changed, treatment algorithms shifted to reflect completely different approaches to old and new choices, and further advances in tyrosine kinase 412inhibitor therapy continue to morph approaches to the treatment of CML and Philadelphia chromosome positive (Ph(+)) leukemias as a whole.