TP53 and pancreatic ductal adenocarcinoma: A recent study in a mouse model of pancreatic ductal adenocarcinoma further showed that the inactivation of p53 does not merely open a gateway to genetic chaos but, rather, can enable a predictable pattern of cancer genomic development (i.e., accumulation of deletions, genome doubling, and the emergence of gains and amplifications), suggesting that p53 and its inactivation play a deterministic role in the ordered development of CIN in cancer6.