Most of the currently existing transgenic mouse models of pancreatic carcinogenesis produce only acinar-ductal metaplasia and ductal proliferation, with zero or very low penetrance of developing frank pancreatic tumors, unless the transgenic mice are concomitantly deficient in certain tumor suppressor genes such as Ink4/Arf or p53 [43-49]. This evidence concerns the gene CDKN2A and neoplasm.