With this as a background we propose that the TL1A/DR3 axis may represent an important mediator of the chronic inflammation taking place in the lung of patients with sarcoidosis, similarly to what has been recently demonstrated in other Th1/Th17 chronic disorders as Chron’s disease, in which TL1A/DR3 account for IFN-γ and IL-17 increasing, intestinal Treg proliferation, and, in a murine model, for the development of collagen deposition [29]. The gene discussed is TNFRSF25; the disease is sarcoidosis.