Stimulation of cells with NF‐κB‐activating ligands such as the cytokine tumor necrosis factor (TNF) results in the degradation of IκBα, and then NF‐κB translocates to the nucleus, where it regulates transcriptional programs.[7] Studies have shown that NF‐κB signaling is constitutively activated in almost 70% of pancreatic cancer specimens[8] and plays a crucial role in PDAC development, progression, and resistance.[9]. This evidence concerns the gene NFKB1 and pancreatic neoplasm.