For example, in PCa cell lines, RB1 loss enhanced ionizing radiation-induced DNA damage and promoted cellular senescence through a TP53-dependent pathway, but double deletion of RB1 and TP53 reversed DNA damage-induced cellular senescence and promoted radiation survival, although radiosensitivity could be restored by PARP1 inhibitor treatment [38]. The gene discussed is RB1; the disease is posterior cortical atrophy.