For example, the combination of PARP inhibitor Veliparib and HDAC inhibitor SAHA synergistically caused synthetic lethality in prostate cancer cells [250], whereas the combination of PARP inhibitor Niraparib, HDAC inhibitor Romidepsin or Panobinostat, and a hypomethylating agent Decitabine induced apoptosis in human leukemia and lymphoma cells through trapping PARP1 and DNMT1 onto the chromatin, enhancing the acetylation of DNA repair proteins and downregulation of NuRD [251]. The gene discussed is HDAC9; the disease is prostate carcinoma.