Since the increased formation of superoxide anions by NOX2 activation promotes ET-1 reduction in the endothelium [25], suggesting a putative link between the NOX2 activation and ET-1 expression, we speculated that the reduction in ET-1 levels in the endothelium might represent a compensatory response to modulate and counteract the oxidative stress and endothelial dysfunction observed in this context. Here, EDN1 is linked to endothelial dysfunction.