These findings suggested that excessive production of KC following viral infection might contribute to the susceptibility of SJL mice to the development of TMEV-induced demyelinating disease, as seen from the effects of IL-1β, IFN-α/β, or TLR3 signaling (Jin et al., 2010, 2011; Kim et al., 2012). The gene discussed is TLR3; the disease is demyelinating disease.