Previously, this approach has predicted the resistance mechanisms that occur clinically in many instances, including erlotinib-resistance in EGFR mutant lung cancer, imatinib-resistance in BCR-ABL translocated leukemia, resistance to Smoothened inhibitors in Patched1-deficient medulloblastoma, and resistance to ALK inhibitors in ALK-translocated lung cancers [23-28]. Here, ALK is linked to leukemia.