Neutralization of IFN-γ or administration of IFN-γ–deficient donor T cells in the B6 to B6D2F1 model under nonirradiated conditions resulted in delayed GVHD-induced mortality that was associated with impaired cytotoxic T lymphocyte (CTL) function, reduced elimination of host cells, enhanced Th2 differentiation, and chronic GVHD-like features when compared with recipients of WT grafts (53). The gene discussed is IFNG; the disease is chronic graft versus host disease.