Corroborating to this point, other lines of evidence also suggest that while inducible extinction of Kras in genetically engineered mouse models results in complete regression of pancreatic tumors in the short term, a subset of those tumors recur in the long term by escaping Kras oncogenic addiction through a YAP1-mediated transcriptional program (23). Here, KRAS is linked to pancreatic neoplasm.