The co-occurrence of thoracic aortic aneurysm and aberrant vertebral artery perfusion (right vertebral artery supplying the left subclavian artery and descending aorta) suggests a mechanistic model where MYLK-mediated contractility defects and FBN2-dependent elasticity impairment act additively to disrupt vascular mechanohomeostasis (Humphrey and Schwartz, 2021). The gene discussed is MYLK; the disease is thoracic aortic aneurysm.