APOE and atherosclerosis: Recent studies have suggested that loss of peroxiredoxin 1 (Prdx‐1), a member of a ubiquitous family of antioxidant enzymes,40 reduces endothelial cell activation and early atherosclerosis.41 Because an increase in Prdx‐1 expression could contribute to the observed cytoprotective effect of TDAG51 deficiency against oxidative stress (Figure 9B), lesions from dKO and ApoE−/− mice were immunostained for Prdx‐1.