ANGPT2 and Sepsis: These results illustrate (a) the presence of a serum activity during severe sepsis that induces endothelial barrier disruption; (b) that clinical resolution correlates with falling Ang-2 and decreased barrier-disrupting activity; and (c) that this activity can be reversed with Ang-1, suggesting that Ang-2 in the serum of human patients is at least partially responsible for altering endothelial architecture in sepsis.