This caused increased production of IFN-I and enhanced infiltration of CD8+ cytotoxic T lymphocytes (CTLs), which resulted in an improved response to anti-programmed cell death protein-1 (PD-1)/anti-PD-L1 in patients with EGFR-mutant lung adenocarcinoma (LUAD). Here, PDCD1 is linked to lung adenocarcinoma.