PDAC and its most common precursor lesions, pancreatic intraepithelial neoplasias (PanINs), are thought to mainly originate from tubular complexes (TC) formed in the centroacinar-acinar compartment through a reprogramming process named acinar-to-ductal metaplasia or through the proliferation of centroacinar cells.2 The KRAS gene is found mutated (KRASG12D) almost ubiquitously in PDAC and PanIN lesions3 and is considered the key driver oncogene in pancreatic cancer initiation. Here, KRAS is linked to familial pancreatic carcinoma.