A model for G-CSF–induced mobilization by the cooperative regulation of the SNS and erythroblasts. The SNS-mediated suppression of the microenvironment, such as osteolineage cells and macrophages, generates a “ready-to-be-mobilized” state for HSCs/HPCs. G-CSF, probably via SNS, induces BM hypoxia, which triggers the release of FGF-23 mainly from erythroblasts (and also partially from stromal cells). The residual anchoring pathway, chemoattraction toward CXCL-12⁺ cells, such as CAR cells, is suppressed by the high concentration of BM FGF-23, which counteracts the CXCR-4 function via FGFRs.