The clinical application of PD-L1/PD-1 blockade therapies was thought to prevent tumor progression by “removing the breaks” in T cells.1 However, other factors apart from “removing breaks” in T cells influence the efficacy of PD-L1/PD-1 blockades, including interferon signatures within the tumor.78–80 Indeed, a functional interferon signal transduction pathway in cancer cells is required for the clinical efficacy of PD-L1/PD-1 blockade agents. The gene discussed is CD274; the disease is neoplasm.