In apolipoprotein (Apo)E knockout (−/−) mice that develop a disease similar to human atherosclerosis, NOX activator-1 is increased in aortic atherosclerotic lesions [10], and double ApoE−/−/NOX1−/− mice show reduced O2•− in the heart and atherosclerotic lesions vs. ApoE−/− animals [3,12,13] (Table 1). The gene discussed is APOE; the disease is atherosclerosis.