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]. The gene discussed is SMAD4; the disease is pancreatic adenocarcinoma.