Chronic myeloid leukemia(CML) is a myeloproliferative disease which leads the unregulated growth of myeloid cells in the bone marrow. It is characterized by the presence of Philadelphia chromosome. Reciprocal translocation of the ABL gene from chromosome 9 to 22 t(9; 22)(q34; q11.2) generate a fusion gene(BCRABL). BCR-ABL protein had constitutive tyrosine kinase activity that is a primary cause of chronic phase of CML. Tyrosine kinase inhibitors(TKIs) are now considered standard therapy for patients with CML. Even though, successful treatment with the TKIs, allogeneic stem cell transplantation(ASCT) is still an important option for the treatment of CML, especially for patients who are resistant or intolerant to at least one second generation TKI or for patients with blastic phase. Today, we know that there is no evidence for increased transplantrelated toxicity and negative impact of survival with pretransplant TKIs. However, there are some controversies about timing of ASCT, the optimal conditioning regimens and donor source. Another important issue is that BCRABL signaling is not necessary for survival of CML stem cell and TKIs were not effective on these cells. So, ASCT may play a role to eliminate CML stem cells. In this article, we review the diagnosis, management and treatment of CML. Later, we present our center’s outcomes of ASCT for patients with CML and then, we discuss the place of ASCT in CML treatment in the TKIs era. Chronic myeloid leukemia (CML) is a myeloproliferative disease which leads the unregulated growth of myeloid cells in the bone marrow. Reciprocal translocation of the ABL gene from chromosome 9 to 22 t (9; 22) (q34; q11.2) generate a fusion gene (BCRABL). BCR-ABL protein had constitutive tyrosine kinase activity that is a primary cause of chronic phase of CML. Tyrosine kinase inhibitors (TKIs) are now considered standard therapy for patients with CML Even though, successful treatment with the TKIs, allogeneic stem cell transplantation (ASCT) is still an important option for the treatment of CML, especially for patients who are resistant or intolerant to at least one second generation TKI or for patients with blastic phase. Today, we know that there is no evidence for increased transplant toxicity and negative impact of survival with pretransplant TKIs. However, there are some controversies about timing of ASCT, the optim al conditioning regimens and donor source. Another important issue is that BCRABL signaling is not necessary for survival of CML stem cells and TKIs were not effective on these cells. So, ASCT may play a role to eliminate CML stem cells. In this article, we review the diagnosis, management and treatment of CML. Later, we present our center’s outcomes of ASCT for patients with CML and then, we discuss the place of ASCT in CML treatment in the TKIs era.