In recent years, the DR-3/TL1A axis has emerged as a key regulator of inflammation and autoimmunity in its own right, with in vivo studies of transgenic mice deficient for DR-3 or TL1A and those overexpressing TL1A or dominant-negative forms of DR-3 providing compelling evidence for an essential role of the DR-3/TL1A axis in many models of inflammatory and autoimmune disease (12–22). The gene discussed is TNFRSF25; the disease is autoimmune disease.