In summary, our study found that high bisecting GlcNAc modification not only promoted the PD-L1 degradation, but also inhibited the binding of PD-L1 to PD-1, thereby enhancing CD8+ T cell-mediated cytotoxicity, and improving the PD-L1 mAb sensitivity, presenting a certain theoretical basis for bisecting GlcNAc modification as a potential therapeutic target in BC. The gene discussed is CD8A; the disease is breast cancer.