This included the apparent greater protection against experimental autoimmune encephalomyelitis afforded to DR‐3−/− mice 38 compared to TL1A−/− mice 42 in otherwise similar models of disease and the DR‐3–independent triggering of TNFRII expression by TL1A in kidney organ cultures 43. Here, TNFRSF25 is linked to experimental autoimmune encephalomyelitis.