As in RA and SLE, it is probable that engagement of TLRs activates inflammatory cells and promotes secretion of pro-inflammatory cytokines, such as IL-6, TNFa, and type I IFNs, which not only drive inflammation in AS, but also could further activate macrophages in the atherosclerotic plaques and thus promote atherogenesis. The gene discussed is TNF; the disease is rheumatoid arthritis.