ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive: TKIs, which originally inhibited the activity of BCR-ABL1 fusion gene product, have been performing an extremely important role in CML patients.[1] In addition to the characteristic chromosomal aberration, studies related to additional clonal chromosomal abnormalities in Philadelphia-negative cells (CCA/Ph–) of CML after TKI therapy have been reported in a small subset of patients, and the ratio related to imatinib is 2% to 17%.[2,3] Some of the CCA/Ph–in CML are transient, whereas others persist,[4] and the influence of CCA/Ph−on the clinical course of CML is controversial.