Our findings that C3aR deficiency did not alter arthritis severity in mice with hematogenous septic arthritis, however, strongly support the conclusion that, compared to the opsonization effect of C3b, the involvement of C3a/C3aR-mediated proinflammatory processes plays only a minor role in the development of septic arthritis. The gene discussed is C3AR1; the disease is arthritic joint disease.