Furthermore, cordycepin treatment in the experimental autoimmune encephalomyelitis (EAE) mice model decreased the level of chemokines (CC chemokine ligand 6 (CCL6), PAR response elements 2 (PARRES-2), IL-16, C-X-C motif chemokine ligand 10 (CXCL10), and cc motif chemokine ligand 12 (CCL12)) in the CNS and spinal cord and inhibited the production of pro-inflammatory cytokines (IFN-γ, IL-6, TNF-α, and IL-17) in activated microglial cells, macrophages, and Th cells in vitro [174], thus potentially ameliorating MS progression. This evidence concerns the gene CXCL10 and experimental autoimmune encephalomyelitis.