The specific reasons for this are as follows: studies have shown that downregulation of PD-L1 can reduce radioresistance by promoting apoptosis, the combination of radiotherapy and anti-PD-L1 antibody in mouse models synergistically improves antitumor immunity by promoting CD8+ T cell infiltration and reducing the accumulation of MDSCs and tumor-infiltrating regulatory T cells and PD-L1 can be maintained through phosphorylation of OCT4 and Nanog stemness of breast cancer cells [16]. This evidence concerns the gene CD274 and breast carcinoma.