The TGFβ-Alk5 pathway is important for the shear stress response (15–17), and recent work has shown that endothelial-specific deletion of both TGFβR1 (Alk5) and TGFβR2 delayed atherosclerotic plaque growth and induced regression of fully established lesions, thus clearly establishing a causal relationship between EndMT and atherosclerosis (18). This evidence concerns the gene TGFB1 and atherosclerosis.