TGFβ-Alk5 signaling is critical for the reaction to shear stress (Egorova et al., 2011b), and emerging evidence has revealed that endothelial-specific deletion of both TGFβR1 (Alk5) and TGFβR2 retards the outgrowth of atherosclerotic lesions and causes complete remission of well-established plaques, demonstrating a clear cause-and-effect connection of EndMT to atherosclerosis (Frutkin et al., 2009). The gene discussed is TGFBR1; the disease is atherosclerosis.