In the setting of hyperglycemia, ER prevented ROS production, downregulated expression of inflammatory mediators (NF-κB, NADPH oxidase p22phox, COX-2, TNF-α and IL-6), inhibited caspase 3/7 activation, averted endothelial hyperpermeability, and preserved endothelial tight junction function (increases expression of vascular endothelial-cadherin (VE-Cadherin) and zonula occludens-1 (ZO-1) proteins, which are cell-cell contact proteins) [101]. The gene discussed is CDH5; the disease is Hyperglycemia.