The discovery of synthetic lethality due to the combined loss of PARP1/inhibition of PARP1 with a PARPi and BRCA1/2 defect has revolutionized the treatment of DNA-repair-deficient cancers mainly in ovarian, breast, prostate and pancreatic cancers and has resulted in the development of a number of PARP inhibitors namely olaparib, niraparib, rucaparib, talazoparib and veliparib across different tumour types [12,13]. This evidence concerns the gene BRCA1 and familial pancreatic carcinoma.