Dear Editor,Chronic myeloid leukemia (CML) is a malignant hematopoietic stem cell proliferative disease driven by BCR-ABL tyrosine kinase,the product of the Philadelphia chromosome[1].Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of CML.Such molecule directed against BCR-ABL firsrt introduced into clinical practice was imatinib mesylate (IM,Gleevec/Glivec,formerly STI571),which showed excellent efficacy in terms of prolonged major molecular response (MMR) and progression-free survival[2].Replacing hematopoietic stem cell transplantation,IM is currently recommended as the first-line therapy for CML by the National Comprehensive Cancer Network (NCCN) and European Leukemia Net (ELN).At the pre-TKI stage,IFN-α was the major choice for CML patients who were not candidates for allogeneic stem cell transplantation,and its observed complete cytogenetic response (CCyR) rates were approximately 20％.Moreover,IFN-α extends the leukemia-free survival (LFS) of patients[3,4].In China,many patients begin with IFN-α treatment instead of IM at diagnosis for economic reasons.Previous studies have shown that the therapeutic efficacy of IM treatment is not affected by prior IFN-α treatment[5,6].The results of our retrospective analysis of 137 CML cases suggest that IFN-α treatment before IM therapy is a risk factor associated with loss of MMR.