Tissue damage, infections or flogosis induce the exit of stem cells from the BM to contribute to tissue repair.32 Disruption of the CXCR4/CXCL12 axis in the BM, which can be directly achieved by CXCR4 antagonists or indirectly by G-CSF through the development of a proteolytic enviroment, increases the motility of hematopoietic stem cells and their egress from the BM.33 The gene discussed is CXCR4; the disease is infection.