Chronic myeloid leukemia (CML) is a paradigm for neoplasias that are defined by 
a unique genetic aberration, the BCR-ABL1 fusion gene. CML is also the best 
example for molecular target therapy. The development of protein tyrosine kinase 
inhibitor, imatinib, has entirely changed the strategy of therapy for CML. 
Nonetheless, many fields of pathogenesis for CML have not been elucidated, such 
as the mechanisms of blastic crisis, the causes of genetic instability including 
the inactivation of tumor suppressor genes, and oncogenic signaling pathways 
downstreams of the BCR-ABL1 fusion gene product. Herein, we review current 
knowledge on the molecular pathogenesis of CML.