The development of arthritis in K/BxN serum-transferred mice, a model in which autoantibodies against glucose-6-phosphate isomerase play an important role, is suppressed by the deficiency of factor B, C3, C5 or C5a, but not by C1q or MBP-A, suggesting the involvement of the AP in the pathogenesis5. The gene discussed is GPI; the disease is arthritic joint disease.