As we have previous data demonstrating that the endothelial dysfunction induced by IL1β is due to an increased oxidative stress produced by enhanced NADPH oxidase activity, which is also occurring in diabetes [12], it seems reasonable to conclude that a pathway linking the over-activation of PPP with the NADPH oxidase activity may have a role in several vascular alterations associated to diabetes mellitus. Here, FMO5 is linked to endothelial dysfunction.