Abstract: Chronic myelogenous leukemia(CML) is a type of self-renewal stem cells malignant myeloproliferative disease. PH chromosome which is an abnormal chromosome can be detected in about 90% patients with peripheral blood. Part of BCR gene from chromosome 22 is fused with the ABL gene on chromosome 9, resulting in formation of BCR-ABL fusion gene, a new gene sequence. The protein p210 which is encoded by this abnormal fusion gene could enhance the activity of tyrosine kinase, resulting in the inhibition of apoptosis. The action of the BCR-ABL protein is the pathophysiologic cause of chronic myelogenous leukemia. Imatinib is the first approved drug of BCR-ABL kinase inhibitor. However, multiple drug resistance of tumor cells against imatinib has emerged due to the mutations in the BCR-ABL kinases. To overcome imatinib resistance, the second generation BCR-ABL inhibitors were developed, including multi-target kinase inhibitors. Although these inhibitors have been proved to be effective against most mutations of BCE-ABL except T3151. Subsequently, the third generation BCR-ABL kinase inhibitors targeting T3151 mutation have been developed. These inhibitors could be used as single agent or combined with other drugs. Some efforts have been performed to increase the inhibitor selective and reduce adverse side effects. With developing from the single target to multi targets, BCR-ABL inhibitors could inhibit wild type and mutanted BCR-ABL kinases. The recent progress in research on high selectivity and more potent BCR-ABL inhibitors is ongoing.