Previous studies have revealed that Treg-mediated suppression of the immune response is abrogated by triggering GITR [13, 16] and high levels of sGITRL or sGITR in serum have been reported in autoimmune diseases, such as rheumatoid arthritis (RA), Hashimoto’s thyroiditis, systemic lupus erythematosus (SLE), and Sjögren’s syndrome (SS) [17–20]. Here, TNFRSF18 is linked to rheumatoid arthritis.