Autoantibodies against complement components were found in RA patients, including C1q (32, 33), factor H (FH) (34) and mannose binding lectin (MBL) (35), further confirming the involvement of the three complement pathways in the pathomechanism of RA, although the functions and relevance of these autoantibodies were not investigated and are still unknown. This evidence concerns the gene MBL2 and rheumatoid arthritis.