In this study, we found in FLT3mut AML that (1) MIF, a tumor-promoting cytokine, was released in greater amounts after TKI-treatment; (2) CXCR2, a receptor for MIF and many pro-inflammatory cytokines was increased by TKI-treatment; (3) NFKB2-MIF/CXCLs-CXCR2 signaling pathways could be responsible for the survival of TKI-treated FLT3mut AML blasts (Figure 7); and (4) The combination of GILT and NFKB-I can effectively treat primary blasts by reducing tumor-promoting cytokines ex vivo. Here, CXCR2 is linked to neoplasm.