In in vivo experiments, mouse models with T cell‐specific knockout Socs1 demonstrated that loss of Socs1 in T cells enhanced T cell proliferation ability, increased secretion of the proinflammatory cytokine IFN‐γ, exacerbated GVHD‐induced target organ damage, and shortened the life span of GVHD mice. Here, IFNG is linked to graft versus host disease.