Knockdown of cGAS or STING in multiple breast cancer cell lines severely compromised IFNβ release in response to IR in vitro and reduced systemic tumor control of bilateral flank models following IR and anti-CTLA4 treatment, demonstrating the importance of intact cGAS-STING-type I IFN signaling in tumor cells for optimal efficacy [25]. The gene discussed is STING1; the disease is breast carcinoma.