The stronger suppression of antiviral immunity by 4-OI in cancer cells can be attributed to several factors, including the molecule’s penetrance in cancer versus normal cells, the binding affinity of different targets (such as MAVS, JAK1, IKKβ) to 4-OI in normal/cancer cells, and the magnitude of the immune response to VSVΔ51 that the drug must overcome in normal/cancer cells. This evidence concerns the gene MAVS and cancer.