Moreover, when the expression of endogenous antagonist angiopoietin-2 (Ang-2) is increased, it displaces ang-1 from the endothelium-stabilizing receptor Tie2 in sepsis, inducing heightened heparanase expression, thus stimulating pathogenic sheddase of the endothelial glycocalyx [30,61]. This evidence concerns the gene HPSE and Sepsis.