Therefore, our data correlate well with the known roles of TLR7and -9 in lupus pathogenesis, and suggest an exacerbating cycle in lupus patients: EBV infection induces TLR7 expression; TLR7 activation promotes LMP1 expression; LMP1 might potentiate the cells for IFN production by TLR3 and TLR9 agonists; and high amounts of IFNs would promote more auto-antibody productions, cell/tissue damages, and eventually more self-nucleotide complexes to activate TLRs [75], [76], [77], [78], which may again promote LMP1 expression (Figure 6). The gene discussed is TLR9; the disease is Epstein-Barr virus infection.