Another mechanism of atherosclerosis prevention may be related to anti-inflammatory effects, and it was shown that estradiol can regulate monocyte chemotactic protein-1 (MCP-1) in human coronary artery smooth muscle cells [39], increase prostacyclin synthesis in cells from atherosclerotic lesions [40], impair endothelial function in postmenopausal women [41], transform growth factor activity [42], and attenuate atherogenesis via selective estrogen receptor beta modulator 8β-VE2 [43]. The gene discussed is ESR2; the disease is atherosclerosis.