The increased expression of CX3CL1 in CSF and serum of MS patients, the enrichment of CX3CR1+CD4+ cells within CSF and MS lesions, and the proinflammatory effect of fractalkine on cytokine secretion and upregulation of the adhesion molecule suggest that its induction of inflammatory cell migration may represent an attractive therapeutic target. This evidence concerns the gene CX3CR1 and myeloid sarcoma.