While IFN-β enhance cross-priming of dendriticcells and support survival of newly activated cytotoxic T lymphocytes(CTLs), it can also up-regulate PD-L1on tumor cells through both IRF9-dependent and independent pathways. Thus, we hypothesized that R.E-induced IFN-βwould stimulate antitumor immunity and transform a cold TME into ahot one, whereas the concurrent increase in PD-L1 could impose anadaptive inhibition on the function of CTLs. The gene discussed is IFNA1; the disease is neoplasm.