Oncogenic KRAS accelerates this process in pancreatic tissue (Figure 1) [13,14,15], inducing, along with inflammatory damage (e.g., cerulean-induced pancreatitis) and other tumor suppressor deficiencies (e.g., protein (p)16INK4a/p14ARF, Tumor Protein p53 (TP53) and/or Suppressor of Mothers against Decapentaplegic 4 (SMAD4)) loss, the appearance of neoplastic precursor lesions, such as acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN) [15]. This evidence concerns the gene TP53 and pancreatitis.