Induction of experimental autoimmune encephalomyelitis (EAE) on a mouse model of CX3CR1 hypofunction by replacement of the normal mo Cx3cr1 locus for the hu Cx3cr1-I249/M280 variant, revealed exacerbated functional signs of EAE, with more severe inflammation and neuronal loss (Cardona et al., 2018). The gene discussed is CX3CR1; the disease is experimental autoimmune encephalomyelitis.