Considering the presence of oncogenic KRAS mutations leads to the overexpression of various cytokines and chemokines and inhibition of tumor-intrinsic interferon (IFN) signaling, thereby forming an immunosuppressive tumor microenvironment and ultimately promoting immune evasion of cancer cells [54, 55], combining immunotherapies may hold significant promise for the treatment of KRAS-mutant CRCs. This evidence concerns the gene IFNA1 and neoplasm.