KRAS and pancreatic neoplasm: By comparing the extracted data on the molecular profiles of ITPN with the existing datasets of pancreatic tumors, the classic pancreatic drivers of PDAC/IPMN, such as KRAS, TP53, CDKN2A, SMAD4, GNAS, and RNF43, were significantly less altered in ITPN than in PDAC/IPMN (P < 0.001), whereas the MCL amplifications, FGFR2 fusions, and PI3KCA mutations were significantly more common in ITPN than in PDAC/IPMN (P < 0.001).