Thus, our finding that CTX treatment activates the cGAS–STING–IFN-I axis in BM-derived cells of mice with advanced breast cancer indicates that CTX bypasses the IFN-I defect of tumor cells, implying that CTX can be successfully deployed to treat CIN tumors that account for more than 90% of solid tumors [50]. The gene discussed is STING1; the disease is neoplasm.