An impairment of critical complement functions caused by variations in genes for complement proteins has been associated with increased susceptibility to several inflammatory and autoimmune diseases, such as age-related macular degeneration (AMD), systemic lupus erythematosus (SLE), atypical hemolytic uremic syndrome (aHUS), and rheumatoid arthritis (RA) (4, –6). Here, VTN is linked to rheumatoid arthritis.