According to these findings, it was proposed that: (a) familial precursor lesions of pancreatic adenocarcinoma do not start through the inactivation of a tumor suppressor gene; (b) KRAS mutations usually precede tumor suppressor gene inactivation in precursor lesions; (c) among the precursor lesions that displayed copy number alterations, there is no one common tumor suppressor locus targeted [25]. Here, KRAS is linked to pancreatic adenocarcinoma.