Neutralization of endogenous Ang2 via an antagonistic monoclonal anti-Ang2 antibody significantly improved survival in our sepsis model (Fig. 1D), and co-administration of exogenous Ang2 diminished the protective effect of exogenously administered Ang1 (Fig. 1E), indicating that Ang2 functioned as a competitive antagonist to Ang1 in our neonatal sepsis model11. The gene discussed is ANGPT1; the disease is Neonatal sepsis.