Pre-clinical evidences suggested that activation of EGFR would up-regulate the expression of PD-L1 through numerous signaling pathways, including p-ERK1/2/p-c-Jun and JAK/STAT3, and blockade of PD-1 would improve the survival of murine models with EGFR mutated lung adenocarcinomas by promoting T cell infiltration and down-regulating pro-tumorigenic cytokines (4–6). Here, EGFR is linked to lung adenocarcinoma.