Additionally, complement receptor 1 (CR1 or CD35), complement receptor 2 (CR2 or CD21), complement receptor 3 (CR3 or CD11b/CD18), complement receptor 4 (or CD11c/CD18), and complement inhibitors such as FH, decay-accelerating factor (DAF or CD55), membrane cofactor protein (or CD46), and protectin (CD59) have been shown to play an important role in the complement-mediated injury and also, as we will discuss below, in the pathogenesis of arthritis. This evidence concerns the gene CR1 and arthritic joint disease.