For instance, MYLK nonsense mutations have been reported to disrupt the kinase domain of MLCK via premature termination of translation, resulting in insufficient phosphorylation of myosin light chains and failure of smooth muscle cell contraction, thereby predisposing to thoracic aortic aneurysms and dissections (Luyckx et al., 2017). This evidence concerns the gene MYLK and thoracic aortic aneurysm.