These results suggested a theoretical model where AD-related neuronal pathologies observed in Bmi1-deficient mice are triggered in part by a ATM/ATR-driven DDR working upstream of p53, but where Bmi1/Ring1 ubiquitin ligase activity and Bmi1-mediated ROS repression are also likely required to prevent p53 accumulation (Fig. 6g)52. The gene discussed is ATR; the disease is Alzheimer disease.