The role of persistent host T-cells mediating acute GVHD by interaction with donor APCs has been noted in murine models and in alloHCT transplant patients with increased IFNγ–secreting CD4+ T-cells in skin GVHD biopsies compared to healthy controls, as well as an increased monocyte population with upregulation of chemoattractant receptors and IFN-response genes (IFITM1 and GBP1) compared with healthy controls (77). Here, IFNG is linked to acute graft versus host disease.