Overall, our results explain how a rapid egress of bone marrow-resident monocytes is controlled by chemokine receptor crosstalk in the bone marrow niche where stromal cells and leukocytes form intricate networks, and suggest the antagonism of CXCR4 signaling as a promising therapeutic approach to treat monocytopenia. The gene discussed is CXCR4; the disease is Decreased total monocyte count.