At the luminal interface, MMP-9-mediated proteolysis accelerates endothelial glycocalyx degradation, impairing mechanosensory and anti-thromboinflammatory functions while exposing underlying adhesion molecules that promote leukocyte–endothelial interactions; in patients with hemorrhagic fever with renal syndrome, circulating MMP-9 levels correlated with markers of glycocalyx degradation and organ injury, and mechanistic study identified MMP-9 as a mediator of eGLX shedding in vitro and in vivo [49]. The gene discussed is MMP9; the disease is hemorrhagic fever.