This paradoxical effect is particularly evident in tumors with low antigenicity, where STING agonist treatment promotes IDO‐mediated immunosuppressive pathways, ultimately dampening antitumor immunity.[90] For instance, studies in a Lewis lung carcinoma (LLC) mouse model demonstrated that STING‐deficient mice exhibited slower tumor growth when challenged with native LLC tumors, compared to tumors expressing neoantigens.[90] These findings may help elucidate why STING agonists demonstrate variable therapeutic efficacy across different cancer types. This evidence concerns the gene STING1 and cancer.