Our data showed that when the type I interferon receptor was blocked by anti-IFNAR1, the concentration of irradiated tumor-released IFN-β in mice serum was eliminated, which might weaken the activation of intratumoral CD8+ T cells and therefore reduced the release of IFN-γ, leading to the inhibition of IR-induced ATAE whether PD-L1 was knocked down or autophagy was inhibited by HCQ. The gene discussed is IFNB1; the disease is neoplasm.