Noticeably, early investigations from our team utilized the CXCR1/2 small-molecule targeted allosteric inhibitor Reparixin, either alone or combined with Ara-C, to intervene in AML cells and explore its mechanism of action on malignant biological behaviors and influence on CXCR family expression; the results indicated that Reparixin combined with low-concentration Ara-C synergistically inhibits AML cell proliferation, invasion, migration, and clonal formation, inducing autophagy and apoptosis pathways. Here, CXCR1 is linked to acute myeloid leukemia.