Although additional studies with a larger cohort of patients are required to determine whether MBL levels associate with the severity of RRV-induced arthritis, and whether this effect reflects a causal role for MBL in human disease, these results, combined with the knockout mouse studies strongly suggest that the MBL pathway of complement activation plays a major role in the pathogenesis of RRV-induced inflammatory disease. This evidence concerns the gene MBL2 and arthritic joint disease.