Diversity in the T cell receptor(TCR) repertoire provides a miniature defense ability for the T cell immune system that may be related to tumor initiation and progression. Understanding the T cell immune status of leukemia patients is critical for establishing specific immunotherapies. Previous studies have reported abnormal TCR repertoires and clonally expanded TCR V? T cells in chronic myeloid leukemia in chronic phase(CP-CML). In this study, we investigated the distribution and clonality of the TCR V? repertoire in 4 cases with imatinib-resistant CML in blast crisis(BC-CML) with abelson murine leukemia viral oncogene homolog 1(ABL1) kinase domain mutations(KDMs). Examination of TCR V? expression and clonality was performed by reverse transcription-polymerase chain reaction(RT-PCR) and Gene Scan analysis. Significantly skewed TCR V? repertoires were observed in BC-CML patients with different KDMs, and 4 to 8 oligoclonally expanded TCR V? subfamilies could be identified in each sample. Intriguingly, a relatively highly expanded V?9 clone with the same length as complementarity-determining region 3(CDR3)(139 bp) was found in all three CML patients in lymphoid blast crisis(LBC-CML) who had different KDMs, but the clone was not detected in the only CML patient in myeloid blast crisis(MBC-CML). In conclusion, restricted TCR V? repertoire expression and decreased clone complexity was a general phenomenon observed in the BC-CML patients with different KDMs, indicating the T-cell immunodeficiency of these patients. In addition, clonally expanded V?9 T cell clones may indicate a specific immune response to leukemia-associated antigens in LBC-CML patients. Diversity in the T cell receptor (TCR) repertoire provides a miniature defense ability for the T cell immune system that may be related to tumor initiation and progression. Understanding the T cell immune status of leukemia patients is critical for establishing specific immunotherapies. Previous studies have reported abnormal TCR repertoires and clonally expanded TCR V T cells in chronic myeloid leukemia in chronic phase (CP-CML). In this study, we investigated the distribution and clonality of the TCR V repertoire in 4 cases with imatinib-resistant CML in Examination of TCR V expression and clonality was performed by reverse transcription-polymerase chain reaction (RT-PCR) and Gene Scan (BC-CML) with abelson murine leukemia viral oncogene homolog 1 (ABL1) kinase domain mutations Significantly skewed TCR V repertoires were observed in BC-CML patients with different KDMs, and 4 to 8 oligoclonally expanded TCR V? subfamilies could be identified in each sample Intriguingly, a relatively highly expanded V? 9 clone with the same length as complementarity-determining region 3 (CDR3) (139 bp) was found in all three CML patients in lymphoid blast crisis (LBC-CML) who had different KDMs, but the clone was not detected in the only CML patient in myeloid blast crisis (MBC-CML). In conclusion, restricted TCR V? repertoire expression and decreased clone complexity was a general phenomenon observed in the BC-CML patients with different KDMs, indicating the T-cell immunodeficiency of these patients. In addition, clonally expanded V? 9 T cell clones may indicate a specific immune response to leukemia-associated antigens in LBC-CML patients.