Cell fluid shear stress and atherosclerotic pathway play an important role in the development of dyslipidemia to atherosclerosis; it has been reported that the wall concentration of lipid in the slow flow area was higher than that in the high-speed laminar flow area, and the action time of lipid and arterial wall was prolonged, which was easy to cause atherosclerosis, and it also can promote oxidative stress, increase the production of ox LDL, upregulate the expression of NF-κB, thus to promote inflammatory response [36, 37]. This evidence concerns the gene NFKB1 and metabolic syndrome.