IFNGR1 and graft versus host disease: Excessive intestinal IFNγ+ T-cell activation is a hallmark of GVHD pathogenesis and drives other inflammatory intestinal diseases, such as immune checkpoint inhibitor-induced colitis.68–70 This may be explained by the capacity of IFNγ to kill ISCs via an on-target effect on IFNγR.26,29,30 Here, we discovered an additional regenerative function of IFNγ that becomes apparent in the context of simultaneous IL-10 activation (Fig. S8).