Contributing factors such as low infiltration of CD8+ tumor‐infiltrating lymphocytes (TILs), low tumor mutational burden (TMB), reduced neoantigen load, and increased presence of regulatory T cells (Tregs) and myeloid‐derived suppressor cells (MDSCs) have been reported.[9, 13, 14, 15] However, these factors alone do not fully explain the compromised efficacy of ICIs in EGFR‐mutant tumors, suggesting that additional immune‐regulatory mechanisms may be at play. This evidence concerns the gene CD8A and neoplasm.