The mechanisms leading to vessel wall damage can be mediated by immune cells and their inducing cytokines, such as interleukin 6 (IL-6) in large-vessel vasculitis [5] or tumoral necrosis factor (TNF) in Behçet disease (BD) [6,7], or by complement activation and/or antibody-mediated toxicity, as seen in systemic lupus erythematosus (SLE) and antineutrophil cytoplasm antibody (ANCA)-associated vasculitis (AAV) [5,8]. The gene discussed is TNF; the disease is anti-neutrophil cytoplasmic antibody-associated vasculitis.