Summary of Cxcl12-deficiency phenotype in adult BM. Loss of Cxcl12 in adult BM resulted in expansion of hematopoietic progenitor pools accompanied with gradual loss of long-term HSCs and excessive cell-cycle entry. In Cxcl12-deficient BM, bone-adhering HSPCs were absent, suggesting a disruption of osteoblastic niche organization. The absence of hematopoiesis from osteoblastic niche was also evident as revealed by the finding that post–5-FU BM regeneration mostly occurred in perisinusoidal space rather than bone-lining surface in Cxcl12-cKO mice.