Highly proliferating cancer cells like BxPC-3 and HPAC greatly rely on BRCA2-dependent HR repair [25], where RAD51-BRCA2/PARP inhibition-based synthetic lethality strategy is effective in eradicating tumour cells, although its impact and outcome may be influenced by TP53 status and DDR machinery regulation and expression (Fig. 2b) [26]. The gene discussed is TP53; the disease is cancer.