In pathological settings, TL1A interactions with DR3-expressing T cells have been shown to play a crucial role in driving inflammatory processes at the site of inflammation in several T-cell-dependent autoimmune disease models, such as rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) [16], [25], [26], [31], [33]–[34]. The gene discussed is TNFRSF25; the disease is rheumatoid arthritis.