However, despite the accumulation of DNA damage in irradiated cells HDAC3-depleted could explain the extraordinary susceptibility of these cells to the activation of death programs, justifying the increase in apoptosis previously described, cancer cells possess the ability to inappropriately activate DDR mechanisms mediated through the activation of HR and/or NHEJ pathways [58], finally leading to cells survival. The gene discussed is HDAC3; the disease is cancer.