A great deal of researches have underlined that bystander T cells recognizing cancer-unrelated epitopes, the presence of suppressive immune cells, insensitivity to interferons or metabolite and cytokine dysregulation in the TME contributed to resistance of ICIs.30 31 Duration IFNγ signaling was also reported to augments adaptive ICIs resistance through inducing overexpression of ISG.RS.20 21 Findings from our experiments showed that SOX2 account for the immune evasion through alleviating the IFNγ signaling and ISG.RS expression. The gene discussed is IFNG; the disease is cancer.