Notch receptors and ligands have been found to be overexpressed in human and mouse PDAC cells, and have been implicated in the progression of pancreatic intraepithelial neoplasia (PanIN) lesions.10, 20, 21, 22 Reports have differed, however, on which specific Notch receptor is central in the progression of PanIN and PDAC lesions, with results supporting Notch1,23 Notch2,21 and Notch3.24 Alternatively, loss of Notch1 in a KRAS‐driven PDAC mouse model resulted in increased tumor incidence and progression, implicating Notch signaling as a potential tumor suppressor.25 The gene discussed is KRAS; the disease is neoplasm.