Septic PMVEC apoptosis and microvascular/PMVEC dysfunction in vivo were both similarly abolished following CLP-sepsis in mice lacking iNOS (Nos2−/−) or NADPH oxidase activity (p47phox−/− and gp91phox−/−), as well as in wild-type mice pre-treated with the NADPH oxidase pharmacologic inhibitor, apocynin. The gene discussed is FMO5; the disease is Sepsis.