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The introduction of imatinib just over ten years ago revolutionized chronic myeloid leukemia (CML) therapy, making long-term survival a reality for the majority of newly diagnosed patients. Unfortunately, residual disease remains detectable in most patients, and even patients with undetectable BCR–ABL (complete molecular response) have a substantial risk of disease recurrence upon discontinuation of imatinib. Studies to understand the mechanism(s) underlying CML persistence in spite of ongoing, successful TKI-based disease management have mainly focused on cell-intrinsic mechanisms.

Blockade of JAK2-mediated extrinsic survival signals restores sensitivity of CML cells to ABL inhibitors