Previous studies have shown that knockdown of Sox17 can lead to impaired cell proliferation of human aortic endothelial cells, and genetic ablation of Sox17 combined with AngII treatment can cause vascular morphological abnormalities and endothelial dysfunction in mice, resulting in an increased occurrence and rupture of intracranial aneurysms in mice [4]. This evidence concerns the gene SOX17 and endothelial dysfunction.