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. The gene discussed is SOCS1; the disease is graft versus host disease.