Xu et al mentioned that OE of PD-L1 induced by IFN-γ could limit the effect of ICIs.32 Additionally, PD-L1 blockade inside tumors was not sufficient to mediate regression, as PD-L1 signaling in defined antigen-presenting cells also inhibited T-cell activation.33 Targeting SOX2 could suppress the JAK-STAT pathway and block the IFNγ-induced ISG.RS OE (including PD-L1) in tumor cells, thus overcome the IFNγ-related resistant to CD8+ T-cell killing and potentiated the effect of anti-PD-1. The gene discussed is PDCD1; the disease is neoplasm.