As described in detail throughout this issue, the Bcr-Abl tyrosine kinase is a well-validated therapeutic target in chronic myeloid leukemia (CML). Present in 95% of patients with CML, Bcr-Abl has been demonstrated to be a leukemogenic oncogene in animal studies and is considered the causative molecular abnormality of CML. Bcr-Abl functions as a constitutively activated tyrosine kinase, impacting numerous signaling pathways. However, all of the transforming activities of Bcr-Abl are dependent on its tyrosine kinase activity (Lugo et al., 1990). Thus, an inhibitor of the Bcr-Abl kinase would be predicted to be an effective and selective therapeutic agent for CML.