Besides, visceral adiposity disturbs the renin–angiotensinogen system and produces excessive reactive oxygen species and reactive nitrogen species, and then induce oxidative stress, which could be presented as oxidized low-density lipoprotein, 8-hydroxylated deoxyguanosine, malondialdehyde, thioredoxin, and advanced oxidation protein products; the oxidative stress would induce a vicious cycle of endothelial dysfunction, inflammation, fibroblast proliferation and affect cerebral arteries through stenosis and occlusion, leading to CVD incidence (38, 41–44). The gene discussed is TXN; the disease is endothelial dysfunction.