In several instances, STING deficiency arises not from genetic alterations, such as mutations or deletions, but rather from epigenetic silencing of STING expression.[26, 28, 43, 44] Our findings demonstrate that HDAC inhibition effectively restores STING signaling in pancreatic cancers through epigenetic reprogramming and reveal that HDACis effectively restore STING expression in pancreatic and breast cancer cells, but not in colorectal cancer cells, in which STING is already expressed, suggesting tumor‐specific vulnerability. Here, STING1 is linked to pancreatic neoplasm.