In LLC flank tumor model, the expressions of cGAS in the flank tumor tissue treated with both ATRi and ablative RT were significantly increased, compared to the control and monotherapy groups (ATRi or ablative radiotherapy), as shown in Fig. 5D. These in vitro and in vivo findings suggest that ATR inhibition enhanced the radiation-induced DAMPs and activated the interferon signaling to trigger the cGAS-STING–p-TBK1–p-IRF3 pathway, thereby stimulating antitumor immunity. The gene discussed is STING1; the disease is neoplasm.