Since first-generation cyclic dinucleotides are transient with a limited membrane permeability, later delivery strategies concentrate STING signaling at the tumor/APC interface, including sustained intratumoral depots/hydrogels for prolonged local exposure, antibody-drug conjugates that ferry STING agonists to tumor or myeloid targets, and endoplasmic-reticulum-targeting constructs that amplify cross-presentation machinery [221–225]. This evidence concerns the gene STING1 and neoplasm.