In an apoE(-/-) murine model, it has been demonstrated that the total atherosclerosis lesions in the whole aorta in apoE(-/-) and p47phox (a key component of NADPH) double knockout mice with either normal or hyperlipid diet was decreased significantly compared to those in the apoE(-/-) mice, indicating that p47phox may be involved in development of atherosclerosis lesion formation [20]. The gene discussed is NCF1; the disease is atherosclerosis.