ACTA2 and coronary artery disorder: The typical response of VSMCs to any type of injury is a change of their phenotype from contractile to synthetic; they rearrange their cytoskeleton, proliferate and lose expression of cytoskeleton stabilizing genes such as Cnn1 and Acta2.[7] The role of VSMC cytoskeleton stabilizing genes is highlighted in patients with mutations in the Acta2 gene or its promoter, leading to a higher risk for coronary disease.[8, 9]