In LN, deposition of C3-containing immune complexes in the glomeruli initiates tissue injury, whereas deficiencies of some of the components of the classical complement pathway, such as C1q and C4, are associated with an increase in the incidence of lupus in humans and also lupus-like disease in C1q or C4 knockout mice118. This evidence concerns the gene C4A and systemic lupus erythematosus.