Building upon these findings and clinical evidence that KRAS inhibitors are able to drive IFN-mediated antitumor immunity through reversing the repression of IRFs in KRAS-mutated cancers 7,39, we propose that the KRAS inhibitors can synergize with concomitant RIG-I activation to amplify the anti-tumor potency in KRAS-addicted cancers. The gene discussed is IFNA1; the disease is neoplasm.