Thus, it is possible that to survive in the hypoxic condition of AML bone marrow, increased release of MIF promotes a favorable tumor microenvironment by restricting the macrophages and performing an autocrine effect to support the survival and proliferation of blasts through both the MIF-CD74/CD44 pathway and the MIF/CXCLs-CXCR2 pathways in relapsed or refractory FLT3mut AML patients (Figure 7). Here, CXCR2 is linked to acute myeloid leukemia.