These studies showed that the absence of S100A8/A9 inhibited the development of joint pathology in antigen-induced arthritis (AIA), whereas the development of other models of experimental arthritis like the K/BxN serum transfer arthritis model and collagen-induced arthritis (CIA) was not affected, suggesting that the importance of S100A8/A9 is model-dependent [6, 28, 29]. This evidence concerns the gene S100A8 and Arthritis.