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. The gene discussed is EGFR; the disease is neoplasm.