Our data also suggest increased TGF-β1 activation in OSS may have clinical implication related to hemodynamic changes seen during atherosclerotic plaque rupture and subsequent thrombosis in myocardial infarctions, where high shear (turbulent/oscillatory) is generated by tissue factor-mediated thrombus formation and platelet activation inside the closing vessels2,4. The gene discussed is TGFB1; the disease is myocardial infarction.