Using previously established cellular models of CCM disease, our group has recently demonstrated for the first time that KRIT1 loss-of-function induces a redox-sensitive upregulation of Glo1, which in turn causes a reduction in intracellular levels of MG-modified cytoprotective chaperone proteins, including heat-shock proteins 70 (Hsp70) and 27 (Hsp27), leading eventually to an increased cell susceptibility to oxidative DNA damage and apoptosis [48]. Here, GLO1 is linked to cerebral cavernous malformation.