Consistent with this idea, systemic administration of a high-affinity inhibitor of CX3CR1 (AZD8797) can effectively block infiltrating CX3CR1+ leukocytes, but not CX3CR1-expressing microglia in the CNS, subsequently relieving clinical symptoms and inhibiting the progression of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis [30]. The gene discussed is CX3CR1; the disease is multiple sclerosis.