Based on our previous studies demonstrating that antagonism of CXCR4 by 1,1′-[1,4-phenylenebis(methylene)]bis[1,4,8,11-tetraazacyclotetradecane] (AMD3100) enhanced functional recovery after experimental stroke [3] we hypothesized that specific CXCR4 antagonism could be a therapeutic target to affect the FKN/CX3CR1 pathway and to modulate microglia function after stroke, to finally improve long-term outcome after permanent focal ischemia. The gene discussed is CX3CR1; the disease is stroke disorder.