Furthermore, and remarkably, this effect was significantly rescued by cell treatment with the antioxidant Tiron, a mitochondria-permeable ROS scavenger previously shown to be effective in rescuing major molecular hallmarks of KRIT1 dysfunctions and CCM disease [20,23], demonstrating that the accumulation of PSSG adducts is indeed a reversible, redox-dependent phenomenon triggered by KRIT1 loss-of-function (Figure 7). Here, KRIT1 is linked to cerebral cavernous malformation.