KRIT1 and cerebral cavernous malformation: While the specific effects of glycative and oxidative post-translational modifications of proteins triggered by loss-of-function mutations of KRIT1, including MG-dependent glycation and S-glutathionylation of important structural and regulatory proteins, remain to be defined, the comprehensive characterization of their upstream regulatory mechanisms and functional interplay should provide novel insights into CCM disease pathogenesis and enable the development of targeted, safe, and effective synergistic drug combination therapies.