Romeo et al. obtained similar results, where the HDAC inhibitor VPA, and trichostatin A (TSA), disrupted the interplay between mutp53 and HSP70, resulting in the downregulation of CHK1 and RAD51, sensitizing pancreatic cancer cells to the AZD2461 PARP inhibitor [20]. The gene discussed is PARP1; the disease is pancreatic neoplasm.