In summary, our data showed that (1) both a FLT3mut AML cell line and primary FLT3mut BMMNC released more MIF after TKI treatment; (2) TKI-treated MV4-11 cells that survived had significantly upregulated gene and protein expressions of CXCR2, a common receptor for MIF and many pro-inflammatory cytokines, which could be a valuable target for immunotherapy to treat FLT3mut AML. This evidence concerns the gene CXCR2 and acute myeloid leukemia.