However, clinical studies of patients with bacterial sepsis have shown that elevations in plasma Ang-2 concentrations precede the appearance of end-organ injury and that serum from patients with sepsis disrupts the integrity of monolayers of endothelial cells in vitro via an Ang-2-dependent mechanism, suggesting that Ang-2 may be directly pathogenic [37]. The gene discussed is ANGPT2; the disease is Sepsis.