The ALK–EGFR–AKT axis promotes STING activation.75 And for the cGAMP-unresponsible spontaneous tumor model, combined usage of the AKT inhibitor can potentiate the antitumor effect induced by cGAMP, while the mechanism was unclear.76 Mutant p53 can bind to TBK1 and prevents the formation of a trimeric TBK1–STING–IRF3 complex.77 This evidence concerns the gene TP53 and neoplasm.