In summary, our data demonstrate a consistent pattern where addition of an MCL1 inhibitor to imatinib strongly and synergistically enhanced the antitumorigenic impact of the TKI on primary human CD34+ CML stem/progenitor cells and on CML cell lines, while the effects of MCL1 inhibitor monotherapy were less conclusive. This evidence concerns the gene CD34 and chronic myelogenous leukemia, BCR-ABL1 positive.