The therapeutic strategy of the combinations of PARP inhibitors with immunotherapies such as anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and anti-programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) has partly been based on the hypothesis that BRCA1/2, and wild-type BRCA1/2 HR deficiency ovarian tumours display a higher neo-antigen load than HR-proficient cancers [41], which in turn produce more effective anti-tumour immune response [19]. Here, PARP1 is linked to neoplasm.