Compared with EGFR/KRAS wild‐type tumors, EGFRmut tumors had lower numbers of predicted MHC‐I and MHC‐II neoantigens.[208] Studies focusing on the EGFR activation and MHC molecules of tumor cells have indicated that downstream PI3K/AKT,[209] MAPK/ERK pathways [210] effectively reduce both MHC‐I and MHC‐II expression. The gene discussed is KRAS; the disease is neoplasm.