In animal models of inflammatory disease including colitis, asthma, arthritis, and experimental autoimmune encephalomyelitis, genetic or antibody-mediated disruption of TNFSF15 signaling through its cognate receptor TNFRSF25 (also known as DR3) generally leads to reduced pathology [29, 54, 59–63], but it is important to remember that these animal studies usually measure disease course and are poor models for disease susceptibility. The gene discussed is TNFSF15; the disease is experimental autoimmune encephalomyelitis.