In particular, our pioneering work demonstrated that the upregulation of Glo1 expression detected in KRIT1-knockout MEF cells and KRIT1-silenced human brain microvascular endothelial cells (hBMEC), two established models of CCM disease, is paralleled by a decrease in the intracellular levels of argpyrimidine (AP), a specific MG-derived protein glycation adduct that plays a dual, context-dependent role in the apoptotic process, acting as either a pro-apoptotic [64,65] or anti-apoptotic factor [99,100]. Here, KRIT1 is linked to cerebral cavernous malformation.