Indeed, deletions of p47phox and gp91phox subunits of NADPH oxidase inhibited superoxide generation in the aorta of ApoE−/− mice, but the effects on atherosclerosis were equivocal [14]–[16]; over-expression of Cu/Zn superoxide dismutase (SOD), which converts superoxide to hydrogen peroxide, did not attenuate atherosclerosis in ApoE−/− mice [17]. The gene discussed is SOD1; the disease is atherosclerosis.