This mutation reduces the infiltration of cytotoxic CD8+ T cells and increases the number of inhibitory myeloid cells, generating an immunosuppressive environment that reduces the efficiency of immunotherapy.186 Additionally, oncogenic KRAS has been linked to the upregulation of CD47, a molecule that helps tumor cells avoid phagocytosis by macrophages, further illustrating the multifaceted ways oncogenes can facilitate immune evasion.187 Moreover, mutations in key oncogenes such as KRAS and STK11 play a significant role in mediating resistance to ICIs in NSCLC. This evidence concerns the gene CD8A and neoplasm.