A common survival strategy in PARP inhibitor-resistant tumor cells is a restoration of BRCA1/2 function through secondary mutations or epigenetic de-repression of BRCA1 or BRCA2, thus restoring the high-fidelity repair of dsDNA breaks by HR DNA repair to escape the synthetic lethality caused by PARP inhibition [49,50]. The gene discussed is PARP1; the disease is neoplasm.