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Abstract Chronic myeloid leukemia (CML) is driven by the constitutively active BCR::ABL1 kinase, which promotes uncontrolled cell proliferation. Although protein-tyrosine kinase inhibitors (TKIs) have revolutionized CML treatment, resistance remains a significant barrier to curative therapy, particularly due to BCR::ABL1 mutations and the persistence of leukemia stem cells (LSCs).
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