The most common mutations found in pancreatic cancer patients are the 6174delT frameshift mutation, 6158insT mutation, splice site mutation 16-2A>G, and the splice site mutation 15-1G>A [52, 110]. BRCA2 inactivation has been reported to be a late event in pancreatic tumorigenesis [111] and suffices to initiate PDAC driven by KRAS mutation G12D or disrupted TP53 [112, 113]. This evidence concerns the gene TP53 and familial pancreatic carcinoma.