CGAS and neoplasm: On the other hand, knockdown AKT1 or targeting AKT1 by MK2206 could release the activity of STING signaling in endocrine‐resistant breast cancer, and on this basis, adding STING agonists maximizes the activation of the cGAS‐STING pathway and blocks the positive feedback loop, which on the one hand changes endocrine‐resistant breast cancer from cold tumors to hot tumors to comprehensively enhance the antitumor immune response and on the other hand reduces the activation of PI3K‐AKT signal to inhibit tumor proliferation, both of which work together to overcome endocrine resistance.