The authors reported that IFN-γ expression was still able to induce resistance when PD-L1 was deleted, but when IFN-γ's receptor IFNGR and the receptor for Type I IFNs IFNAR were knocked out on tumor cells, exhausted T cells were significantly reduced and response to RT and anti-CTLA4 was enhanced (60). The gene discussed is CTLA4; the disease is neoplasm.