It has been revealed that CXCR2 signaling is abnormally activated in response to chemotherapy-induced stress, and the CXCR2 antagonist SB225002 effectively inhibits Ponatinib-resistant CML cell proliferation, induces apoptosis, accumulates reactive oxygen species, and disrupts mitochondrial function, all of which are related to TKI chemotherapy resistance and apoptosis. Here, CXCR2 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.