ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive: TKI resistance in CML patients can be divided into BCR-ABL-dependent and BCR-ABL-independent mechanisms, including BCR-ABL mutations and overexpression, abnormal drug transporter activity, aberrant activation of compensatory signaling pathways, DNA repair and genomic instability, epigenetic dysfunction, durability of LSCs, and immune system dysfunction [27].