Mouse studies unveiled the critical roles of TLR7 in the pathogenesis of SLE, including that (a) its constitutive activation drives systemic autoimmunity (5); (b) deficiency of TLR7 reduces the generation of autoantibodies to RNA-containing antigens and the development of glomerulonephritis (GN) in pristane-induced lupus nephritis (LN) (6); and (c) lupus-prone mice with TLR7 deficiency (Tlr7–/–lpr/lpr) exhibit decreased lymphocyte activation and IgG levels in serum (7). Here, TLR7 is linked to lupus nephritis.