Taken together, these findings suggest that KRIT1 may exert a protective effect against oxidative stress by enhancing the cell capacity to scavenge intracellular ROS through an antioxidant pathway involving FoxO1 and SOD2, thus providing novel and useful insights into the understanding of KRIT1 molecular and cellular functions, and suggesting a novel potential mechanism for CCM pathogenesis. The gene discussed is SOD2; the disease is cerebral cavernous malformation.