Experimental autoimmune encephalomyelitis (EAE) was found to be more severe in CX3CR1-deficient mice [61], but in models for ischemia-reperfusion injury in kidney [62], spinal cord injury [63], and atherosclerosis [64], disease was less severe in CCR2−/− or CX3CR1−/− mice, and attributed to reduced myeloid cell recruitment. This evidence concerns the gene CCR2 and experimental autoimmune encephalomyelitis.