In conclusion, mutated GNAS found in IPMNs may extensively alter gene expression profiles, including expression of mucin genes, as a result of an overactive GPCR signaling pathway and its interactions with the MAPK and PI3K pathways in pancreatic ductal cells; these changes may determine the characteristic phenotype of IPMN. The gene discussed is GNAS; the disease is pancreatic intraductal papillary-mucinous neoplasm.