Mechanism of release of HSCs from the bone marrow microenvironment using G-CSF, plerixafor, or Me6TREN as mobilization agents. G-CSF induces synthesis of proteases elastase, cathepsin, and MMP9 by neutrophils and osteoclasts after binding to G-CSF receptors (G-CSFR). Proteases degrade adhesion molecules that tether HSCs to stromal cells in the bone-marrow microenvironment. As a secondary effect mediated through osteoclasts, G-CSF binding leads to downregulation of CXCL12 on bone-marrow stromal cells. Plerixafor antagonizes binding of CXCR4 to CXCL12, whereas Me6TREN has reported activity in antagonizing CXCR4/CXCL12 binding as well as inducing synthesis of MMP9.