Setting the adequate levels of serum cholesterol is controvertial. Recent basic researches demonstrated the event of atherosclerosis formation: that is, lipid storage making lipid pool, smooth muscle cell proliferation leading to intimal thickninng, inflammatory cell invasion leading to fragility of the matrix, cell apoptosis leading to disappearance of the cell, and plaque rupture. In these process, the chronic inflammatory reaction is insidiously continuing. The most important factor for promoting the inflammatory reaction might be oxysterols, because we found that oxysterols are generated in advanced atherosclerotic lesion, and are very toxic. And, oxidative stress promoted the production of oxysterols. Then, we propose that the atherogenicity is serum cholesterol level times oxidation stress. The latter index was calculated from measuring urinary excretion of 8 hydroxy deoxyguanine. Considering those, total cholesterol level which did not affect to make the progression of atherosclerosis is 140 mg/dl. Oxidative stress in metabolic syndrome was 1.6 times than control. Then, 140×1.6=220 mg/dl might be lower limit involving atheroma formation in standard oxidative stress. If antioxidative stress might be equipped, the limit might be raised. Precise evaluation of oxidative stress might be required.