There may be several explanations for the controversy: 1), TGFβ1 is a bimodal regulator of both endothelial cells and VSMC proliferation, depending on local TGFβ1 levels, cell density, and/or membrane TGFβ receptors[1,2,5,7,8,12]; 2), different pathophysiological stages of CHD may differentially affect the biological effects of TGFβ1[1,3,10]; and 3), circulating TGFβ1 levels may not reflect the real vascular interstitial TGFβ1 levels that are directly involved in the pathogenesis of CHD[3-5,13]. The gene discussed is TGFB1; the disease is coronary artery disorder.