CXCL12 and acute myeloid leukemia: One predominant rationale for targeting the CXCL12/CXCR4 axis in AML and ALL is that its disruption will not only inhibit pro-survival signaling but also mobilize the leukemic cells from the protective bone marrow environment and out into the vasculature where they might be more susceptible to conventional chemotherapeutic agents (Figures 1B,C).