Throughout its history, chronic myeloid leukemia (CML) has set precedents for 
cancer research and therapy. These range from the identification of the first 
specific chromosomal abnormality associated with cancer to the development of 
imatinib as a specific, targeted therapy for the disease. The successful 
development of imatinib as a therapeutic agent for CML can be attributed 
directly to decades of scientific discoveries. These discoveries determined that 
the BCR-ABL tyrosine kinase is the critical pathogenetic event in CML and an 
ideal target for therapy. This was confirmed in clinical trials of imatinib, 
with imatinib significantly improving the long-term survival of patients with 
CML. Continuing in this tradition of scientific discoveries leading to improved 
therapies, the understanding of resistance to imatinib has rapidly led to 
strategies to circumvent resistance. Continued studies of hematologic 
malignancies will allow this paradigm of targeting molecular pathogenetic events 
to be applied to many additional hematologic cancers.