These mutations appear to occur very early in the development of pancreatic neoplasia, as evidenced by the presence of KRAS mutations in noninvasive precursor lesions, including intraductal papillary mucinous neoplasms (IPMN) and PanINs (Hezel et al., 2006; Maitra et al., 2006). Here, KRAS is linked to pancreatic intraductal papillary-mucinous neoplasm.