Although deficiencies of early components of the complement cascade are associated with development of SLE due to their role in clearance of dying cells and tissue debris [7] and their importance in development of tolerance [22], clearance of immune complexes [23] and cytokine regulation [24], activation of complement at later stages of C3 and beyond also contributes to the pathogenesis of SLE. The gene discussed is C3; the disease is systemic lupus erythematosus.