We previously showed that up‐regulation of CXCR4 is associated with increased engraftment and motility of hematopoietic stem cells within the BM microenvironment.7 CXCR4 inhibition prolongs the survival of T‐ALL burdened mice,8 and promotes mobilization and apoptosis of AML cells.9, 10, 11 CXCR4 antagonists in combination with chemotherapy have been tested in phase 1/2 clinical trials in relapsed and refractory AML (reviewed in Cho et al. 12 and Peled et al. 13). The gene discussed is CXCR4; the disease is acute myeloid leukemia.