At the same time, targeting of C5a/C5aR [55–57] and TLR2 [32] has shown promise in experimental models of arthritis and thus the increasing evidence of crosstalk between complement, TLR and IL-1R signalling in inflammatory pathologies such as RA, for example by promoting cellular migration and osteoclastogenesis [59] makes SMAs that potentially target all three convergent pathways an attractive proposition for development of novel treatments for RA. The gene discussed is TLR2; the disease is rheumatoid arthritis.