TWIST1 and atherosclerosis: The canonical function of EndoMT is in the development of valves from EC in the atrioventricular canal21; however, EndoMT has also been implicated in disease processes including cerebral cavernous malformations.44 Of particular relevance, 2 recent studies demonstrated that EndoMT can be induced by disturbed flow and is a driver of atherosclerosis.45,46 Thus, our observation that low shear induces GATA4–TWIST1 signaling provides a molecular mechanism to explain the induction of EndoMT by low shear stress during atherosclerosis.