Our finding that T cells in the accepted kidney allografts increase IFN-γ secretion despite the absence of antigen stimulation corroborates prior studies that showed that IFN-γ abundance drives Tregs to restrain tumor-specific T cell function in tumor-draining lymph nodes or the tumor microenvironment (29, 30), that IFN-γ is secreted by inducible Tregs and has a crucial role in allografts tolerance (31–34), and that CD8+ central memory cells promote tolerance in a murine lung transplantation model through TNF-α– and IFN-γ–mediated mechanisms (35). The gene discussed is IFNG; the disease is neoplasm.