CGAS and neoplasm: In endocrine-resistant ER+HER2- breast cancer, while hyperactivated AKT1 suppresses cGAS-STING signaling by binding to TBK1 and disrupting the TBK1/STING/IRF3 complex, combining AKT1 inhibitors with STING agonists restores innate immune activation and impairs tumor growth in preclinical models (96).