On one hand, the stimulator of interferon genes (STING) pathway, which plays a crucial role in innate immune response to cancer, can be activated at DNA damage repair (DDR) deficiency and exposure to DNA-damaging agents (47), which stimulates interferon (IFN) production and in turn recruit T lymphocytes through the STING-interferon regulatory factor 3 (IRF3) pathway (48, 49), leading to T cell infiltration in HRR gene mutated tumors. The gene discussed is STING1; the disease is cancer.