Despite their potential demonstrated inpreclinical studies, transitioning STING agonists to clinical usepresents challenges.25−27 Notably, the hydrophilic properties of CDNs, coupledwith their susceptibility to rapid enzymatic degradation, attenuatetheir bioavailability, leading to transient and moderate immune activation.While advanced STING-activating agents are being designed to counteractthese limitations with improved bioavailability, they could presentsystemic side effects if they are not targeted to tumor sites. The gene discussed is STING1; the disease is neoplasm.