We then used known pharmacological agents with strong Fli-1–inhibitory activity in preclinical allo-HCT mouse models of acute GVHD (aGVHD) and cGVHD, as well as in a humanized xenograft model of GVHD, and showed that decreasing the expression or activity of Fli-1 may be an important translational concept for reducing the pathogenesis of GVHD without impairing the GVL response. This evidence concerns the gene FLI1 and acute graft versus host disease.