Blocking PD‐1/PD‐L1 signaling has exhibited potent antitumor activities and may obtain a long‐lasting response in various cancers, such as melanoma, non‐small cell lung cancer (NSCLC), RCC, and all microsatellite instability (MSI)‐high cancers.[43, 44, 45, 46] However, the majority of patients do not benefit from ICB therapy, which may be attributed to medium‐high PD‐L1 expression, limiting the revival of antitumor immunity.[47] The molecular mechanism that drives PD‐L1 overexpression remains to be explored. This evidence concerns the gene CD274 and non-small cell lung carcinoma.