It is considered that the inflammatory component underlying ankylosing spondylitis pathological process contributes at least in one part to the overall cardiovascular risk and specifically to endothelial dysfunction, most probably as a consequence of increased proinflammatory cytokines levels, for example tumor necrosis factor alpha (TNF-α), which in turn negatively regulates endothelial function with resulting decrease of endogenous nitric oxide bioavailability [54]. The gene discussed is TNF; the disease is endothelial dysfunction.