TNFRSF9 also has complex effects on different cell types [42, 43], and increased serum levels of soluble TNFRSF9 correlate with disease severity in rheumatoid arthritis and other autoimmune diseases, suggesting that the soluble form may act as a decoy receptor preventing TNFSF9-mediated suppression of T cells [44]. This evidence concerns the gene TNFRSF9 and rheumatoid arthritis.