In addition, extracellular IFI35 and Nmi, as two damage-associated molecular patterns (DAMPs), activated NF-κB pathway via Toll-like receptor 4 (TLR4) from macrophages, leading to the exacerbation of inflammation-related diseases such as lupus nephritis, sepsis and multiple sclerosis (17–19). This evidence concerns the gene TLR4 and multiple sclerosis.