Pharmacological activationof the retinoic acid-inducible geneI (RIG-I) pathway holds promise for increasing tumor immunogenicityand improving the response to immune checkpoint inhibitors (ICIs).However, the potency and clinical efficacy of 5′-triphosphateRNA (3pRNA) agonists of RIG-I are hindered by multiple pharmacologicalbarriers, including poor pharmacokinetics, nuclease degradation, andinefficient delivery to the cytosol where RIG-I is localized. Here, RIGI is linked to neoplasm.