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. The gene discussed is APOE; the disease is atherosclerosis.