While only a single case, this response may imply a synergistic role for C5aR blockade and B-cell mediated depletion therapies and suggests that C5a-mediated neutrophil activation and chemotaxis remains important as a B-cell independent pathway in the pathogenesis of ANCA-associated vasculitis. The gene discussed is C5AR1; the disease is anti-neutrophil cytoplasmic antibody-associated vasculitis.