Specifically, GITR involvement in both innate and adaptive immunity is potentially correlated with the inflammatory activation of autoimmune hepatitis, suggesting that its pharmaceutical inhibition could be considered an effective treatment via inhibiting the activation of T-cells and inflammatory cells and, specifically, via sustaining the immunocompetence of Tregs, leading to autoimmune mechanisms blockade [80]. Here, TNFRSF18 is linked to autoimmune hepatitis.