Ex vivo cultures of CML-derived cell lines and primary CML cells, ectopic expression of BCR-ABL in CD34+ cells and mouse models have provided important insights into CML pathogenesis and led to the development of targeted therapy for this neoplastic disease with BCR-ABL tyrosine kinase inhibitor (TKI), imatinib (Druker et al., 2006; Druker et al., 2001). This evidence concerns the gene CD34 and chronic myelogenous leukemia, BCR-ABL1 positive.