In our model, given that the PK/PD and PARP-1 expression data demonstrate that in olaparib-resistant tumours PARP-1 is still expressed and its enzymatic activity is being inhibited, these tumours may be able to either suppress the DNA damage following PARP-1 inhibition, or repair the damage by re-activating homologous recombination-directed repair (as reported in other studies, although unlikely here considering the nature of the Brca2 recombined allele used in the study) [10], or alternatively tolerate the damage via an as-yet unidentified mechanism. Here, PARP1 is linked to neoplasm.