This is consistent with previous studies, which have found that circulating ADAM10 correlates positively with VE-Cadherin levels in aortic aneurysm and dissection populations; moreover, mechanistic experiments have demonstrated that upregulated ADAM10 increases soluble VE-cadherin levels in cell culture supernatants, whereas ADAM10 inhibition prevents its shedding [38]. The gene discussed is CDH5; the disease is dissection.