Our own recent work has shown that the interaction between KRIT1 and HEG1 can be pharmacologically inhibited, resulting in increased endothelial expression of KLF2, KLF4, and eNOS [15,36], establishing the endothelial CCM complex as a potentially druggable target, with small molecule inhibitors representing a potential therapeutic option for the prevention of endothelial dysfunction in vascular disease. This evidence concerns the gene KRIT1 and endothelial dysfunction.