Accordingly, the deletion of Atm in a mouse model of pancreatic cancer (Atmfl/fl; LSL-KrasG12D/+; Ptf1aCre/+, termed AKC) also causes genomically unstable PDACs, featuring chromosomal instability, disruption of DNA integrity, and aneuploidy, which are indeed sensitive to single PARP inhibitor treatment [10,14,15,16]. This evidence concerns the gene ATM and pancreatic neoplasm.