Normally, HSPCs are retained in BM niches in part by CXCR4/CXCL12 and VCAM-1/VLA-4 signaling (top panel). HSPCs are mobilized by BIO5192's antagonism of VCAM-1, and perhaps in part by suppression of osteoblasts and redistribution of CXCL12 levels via cytokine treatment (bottom panel).