This is consistent with the finding that Prdx‐1 deficiency in ApoE−/− mice causes endothelial activation (increased leukocyte rolling, endothelial P‐selectin, and vWF expression) and accelerates atherosclerosis.41 Further studies should clarify whether TDAG51‐mediated endothelial dysfunction contributes to atherogenesis. This evidence concerns the gene PRDX1 and endothelial dysfunction.