Chronic myeloid leukemia (CML), characterized by the t(9;22) and BCR/ABL1 fusion, is a disease model for studying the mechanisms of genetic abnormalities in leukemogenesis. The detection of the t(9;22), characterization of the BCR/ABL fusion, and the discovery of imatinib have elegantly reflected the success of our research efforts in CML. However, genomic instabilities that lead to the formation of the BCR/ ABL1 fusion are not fully understood. It is important to understand how various genes that are involved in regulating the signaling pathway and epigenetic deregulation cooperate with the BCR/ABL1 fusion in the initiation and progression of CML.