This conclusion was based upon the following findings: (i) radiation upregulated PD-L1 expression in tumor cells in a time- and dose-dependent manner, (ii) radiation activated STAT3 through the production of IFN-γ, which led to PD-L1 upregulation in tumor cells, and (iii) the efficacy of radiation could be increased by combination with anti-PD-L1 antibody, leading to the abrogation of exhausted CD8+ T cells in a murine HCC model. The gene discussed is CD8A; the disease is hepatocellular carcinoma.