Accordingly, over the last decade, it has clearly emerged that KRIT1 loss-of-function predisposes the development of CCM lesions by exerting pleiotropic effects on key redox-sensitive mechanisms involved in cellular homeostasis and defenses against oxidative stress and inflammation, leading to enhanced endothelial cell susceptibility to oxy-inflammatory insults [8,10,12,13,14]. The gene discussed is KRIT1; the disease is cerebral cavernous malformation.