PAAD is known to progress through precursor lesions, primarily pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN), whose genetic evolution involves recurrent driver mutations such as KRAS, TP53, CDKN2A, and SMAD4 [7,8,9]. Here, CDKN2A is linked to pancreatic intraductal papillary-mucinous neoplasm.