Recent evidence suggests that CCL2/CCR2 axis may possibly be involved in AML resistance to chemotherapy, not related to its role in AML migration and proliferation kinetics but related to subsets of immunosuppresive macrophages into the bone, which could be blocked with CCL2/CCR2 inhibitors and that way improve the response to chemotherapy [30]. The gene discussed is CCR2; the disease is acute myeloid leukemia.