The underlying mechanisms driving malignant transformation by CP remain poorly understood.<h4>Objective</h4>Combining a recently developed mouse model of CP carrying the human carboxypeptidase A1 (<i>CPA1</i>) p.N256K mutation with the established <i>Kras<sup>G12D</sup></i> pancreatic cancer model, we characterised mechanisms linking chronic inflammation to early pancreatic carcinogenesis.<h4>Design</h4>We crossed <i>Cpa1</i> <sup><i>N256K</i></sup> mice (Cpa1) with <i>Ptf1a<sup>Cre</sup>;Kras<sup>LSL-G12D</sup></i> (KC). Here, KRAS is linked to pancreatic neoplasm.