These results contrast with studies on mousemodels of diseases, where Sod2 hemizygosity exacerbated diseasephenotypes as (i) increasing the formation of neurotoxic plaques and tangles inAPP and Tg2576 transgenic [57, 58], (ii)reducing the lifespan of G93A transgenic mice - a model for amytrophic lateralsclerosis [59], (iii)increasing diabetic neuropathy in db/db mouse [60], and (iv)increasing endothelial dysfunction in atherosclerosis prone ApoE deficientmice [61]. This evidence concerns the gene SOD2 and atherosclerosis.