It was reported that ROS-mediated activation of p38 mitogen-activated protein kinase (MAPK) plays a pivotal role in the control of differentiation and tumor-initiating capacity of GSCs, and ROS triggered p38-dependent Bmi1 protein degradation and FoxO3 activation in GSCs, which were responsible for the loss of self-renewal capacity and differentiation, respectively [24]. Here, BMI1 is linked to neoplasm.