Mutation in KRAS and MUC was common but not strongly associated with IPMN histologic progression.[19] The malignant transformation of IPMN to an invasive carcinoma depends on the mutations of both P53 and P16.[20] A previous study reported that mutations in GNAS at codon 201 had recently been identified as a hallmark mutation of IPMN.[21] Some reports revealed that GNAS mutation was significantly related to high-grade dysplasia, while others reported that wild-type GNAS was significantly associated with adenocarcinoma.[21,22]. This evidence concerns the gene TP53 and pancreatic intraductal papillary-mucinous neoplasm.