Although increases in ROS have been reported in atherosclerosis, wherein there is increased vascular arginase activity, [11] some of which may be induced by NADPH oxidase-generated ROS, [43] or uncoupled eNOS [44] the results from the present study are aligned with the unchanged eNOS monomer:dimer ratio findings and do not suggest a converse role for arginase in modulating ROS production. The gene discussed is FMO5; the disease is atherosclerosis.