The loss of barrier function observed in the NS1-treated MECs has also been reported in other studies where NS1 was shown to degrade endothelial glycocalyx components [20, 44], increase the secretion of angiopoietin-2 and disrupt the function of junctional protein VE-cadherin [45] in endothelial cells, leading to hyper-permeability and endothelial dysfunction. The gene discussed is ANGPT2; the disease is endothelial dysfunction.