Tim-3 was first described as a TH1-specific inhibitory surface molecule,47 but its expression on other T cell subsets, especially tissue-resident Tregs, as well as on innate immune cells has been described since then.48,49 Tim-3 mediates Treg supressor functions in an AIH model50 and can induce tolerance and the contraction of TH1 effector populations.51 It is described to be increased in the sera of patients with AIH compared with patients with PBC and associated with disease severity.52 The function of soluble Tim-3 is less established. Here, HAVCR2 is linked to autoimmune hepatitis.