Hwang et al. demonstrated that the combination of Ara-C, the CXCR4 inhibitor Plerixafor, and a PD-L1 monoclonal antibody in an AML murine model resulted in a decrease in the number of Tregs and MDSCs in the peripheral blood as well as in bone marrow leukemic cells, inferring that the treatment of AML by modulating the leukemic microenvironment is a very promising strategy [107]. The gene discussed is CXCR4; the disease is acute myeloid leukemia.