In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Parkinson’s disease (PD) mouse model, the deletion of cx3cl1 or cx3cr1 aggravates the dopaminergic neuronal loss and increased microglial activation [57], but the SN injection of recombinant sCX3CL1 in CX3CL1-null mice ameliorated MPTP-induced microglial activation and inflammation, reducing dopaminergic neuronal death and motor impairment; however, treatment with a mutant mCX3CL1 resistant to cleavage has no effect on the MTPT-induced PD phenotype [66]. This evidence concerns the gene CX3CR1 and Parkinson disease.