Our finding that deletion of arginase 2 in mice prevents hyperoxia-induced obliteration of the retinal vasculature while preventing NOS-dependent ROS formation and preserving NO availability is consistent with previous studies showing involvement of excessive arginase 1 in hyperoxia-induced vascular injury in the developing lung [38] and excessive arginase 2 in vascular dyfunction associated with atherosclerosis and aging. This evidence concerns the gene ARG1 and atherosclerosis.