Theoretically, the high PD-L1 expression observed in cells with KRAS mutation results from activation of ERK, which mediates upregulation of PD-L1 [95]; however, the efficacy of ICIs in treating NSCLC tumors harboring EGFR mutations is low, indicating that patients with KRAS but not EGFR mutations are likely to have a good response to ICIs. This evidence concerns the gene EGFR and non-small cell lung carcinoma.