Given that EGFR in most NSCLC patients is activated 35, restricting anti-tumor immune response and ICI efficacy 6, identification of the underlying mechanisms for EGFR-mediated immunosuppression and reshaping the tumoricidal immune microenvironment is urgently needed to maximize the clinical benefit of ICIs in EGFR-activated NSCLC. This evidence concerns the gene EGFR and neoplasm.