We found that targeted inhibition of AKT1 can release TBK1 protein from AKT1 kinase, thereby releasing the activity of the cGAS‐STING pathway in endocrine‐resistant breast cancer cells, indicating that combining STING agonists with AKT1 inhibitors could maximizes the activation of the cGAS‐STING pathway. The gene discussed is CGAS; the disease is breast cancer.