The complement system has been investigated even in the synovial fluid of RA patients, with abundant evidence of complement consumption: increased levels of complement factors (C2, C3, C4, C5, MAC) and complement split products (C3a, C3c, C3d, C4d, C5a, sC5b-C9, C1-C1 inhibitor complexes, Ba, Bb) have been described, suggesting a predominant activation of the classical pathway with the alternative pathway being also activated. The gene discussed is C3; the disease is rheumatoid arthritis.