STING is a critical adaptor for IFN‐I activation, and STING activation in the tumor can remodel the tumor vasculature, leading to increased sensitivity to immunotherapy, [44] and improve cross‐presentation of antigens by STING‐dependent adjuvants.[45] In our animal tumor model, defective STING expression greatly promoted PDAC tumor growth in vivo. Here, STING1 is linked to neoplasm.