In vitro and in vivo studies (uptake, retention and selectivity) of [18F]rucaparib in AsPC1 and PSN1 models, which display different PARP expression levels, suggested that PARP1 remains one of the key players responsible for [18F]rucaparib uptake in cells, although [18F]rucaparib has binding selectivity towards other proteins, leading to higher cellular and tumour uptake compared with the uptake of [18F]olaparib in the same models. This evidence concerns the gene NT5C3A and neoplasm.