In addition, Cxcl1/Cxcl2 also coordinate the mobilization from and the homing back to medullary sites by promoting CXCR4 expression [33] and thus establishing a loop able to control the activity of neutrophils during infections [34], where the balance between “fresh” (i.e. over-expressing CXCR4) and “aged” (CXCR2 bright) becomes critical for the survival of the host. The gene discussed is CXCR4; the disease is infection.