Similarly, the DNA damage response (DDR) inhibition activated the STING/TBK1/IRF3 innate immune pathway, leading to increased levels of chemokines such as CXCL10 and CCL5 that induced activation and function of cytotoxic T lymphocytes (29), while CCL5 recruits T cells in the tumor microenvironment via IFN (11). The gene discussed is STING1; the disease is neoplasm.