We further extended our observations to other DNA damage response inhibitors, including the DNA-PK inhibitor M3814 (peposertib) and the ATR inhibitor AZD6738 (ceralasertib), and found that, similar to AZD1390, neither of the inhibitors in conjunction with radiation induced T1IFN production via the cGAS/STING pathway (Supplemental Figure 1K), further supporting that the cGAS/STING cytosolic dsDNA sensing pathway is dispensable for T1IFN signaling induced by ATM inhibitor and radiation in pancreatic cancer. This evidence concerns the gene ATR and familial pancreatic carcinoma.