Mechanistically, PD contributes to PC development through multiple interconnected pathways: translocation and colonization of periodontal pathogens in pancreatic tissue, induction of precancerous lesions (e.g., acinar-to-ductal metaplasia), activation of inflammatory signaling pathways (TLR4/NF-κB, Wnt/β-catenin), immune dysregulation and tumor immune escape, microbiota imbalance and carcinogenic metabolite accumulation (e.g., acetaldehyde, nitrosamines), and induction of chemoresistance (via cytidine deaminase-mediated gemcitabine inactivation or Notch1 pathway activation). The gene discussed is NFKB1; the disease is neoplasm.