The clinical outcomes of immune checkpoint therapies have revealed that EGFR mutations in lung cancer cells can not only upregulate the intrinsic PD-L1 expression on cancer cells but also suppress T cell function and increase levels of pro-inflammatory cytokines within the TME, which marks an immune escape phenotype of EGFR-mutant NSCLC (Akbay et al., 2013; Chen et al., 2015). This evidence concerns the gene CD274 and lung carcinoma.