The difference may simply be in the number of mice examined, but nevertheless, given that the majority of human pancreatic cancer is presented as well to moderately differentiated ductal adenocarcinoma, it's important that we have demonstrated here that biallelic inactivation of p16 in conjunction with oncogenic Kras in mice mimic human pancreatic tumor progression from PanIN to PDA. Here, CDKN2A is linked to pancreatic neoplasm.