KRIT1 and cerebral cavernous malformation: In summary, our data describe a novel mechanism by which KRIT1 controls the steady-state levels of intracellular ROS, resulting in prevention of cellular oxidative damage, and raise the hypothesis that CCM disease may result from an impaired oxidative stress defense in specific microvascular districts of genetically predisposed subjects, thus paving the way for further research in animal models and CCM patients aimed at defining the role of oxidative stress in CCM pathogenesis.