Editorial Commentary for the manuscript entitled “Docking protein p130Cas regulates acinar to ductal metaplasia during pancreatic adenocarcinoma development and pancreatitis” A p130Cas-mediated mechanism governs acinar to ductal metaplasia and the initiation of pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest cancer types and is predicted to be the second leading cause of cancer-associated mortality worldwide by 2030. Despite the advancement in treatment modalities, the prognosis of PDAC remains poor. Attainment of this long-term goal requires a greater understanding of the molecular mechanisms that regulate the early events of PDAC development. Studies in mouse models suggest that the PDAC originates from acinar cells in response to KrasG12D mutation and is termed acinar to ductal metaplasia (ADM).