Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with a low survival rate. This is notably due to the lack of symptoms during early cancer stages and to the absence of efficient treatments against advance tumors. Understanding mechanisms initiating PDAC is necessary to better understand this disease. Intraductal papillary mucinous neoplasm (IPMN) are precursors lesions of PDAC which evolve in malignant tumors in 36% of cases. As initiating process and tumoral progression of IPMN are poorly characterized, we decided to generate a mouse model allowing to study this lesion. By mutating two genes frequently altered in human IPMN (KRAS and LKB1), we have observed IPMN formation from ductal cells. We have also demonstrated that the formation of these mucinous lesions was dependent of the -catenin activity.