Modeled diseases include supravalvular aortic stenosis (SVAS) accompanied with narrowing or blockage of the ascending aorta and other arterial vessels caused by mutations in elastin (ELN) [168]; congenital cardiovascular malformation associated with bicuspid aortic valve (BAV) defects [169]; Marfan’s syndrome (MFS) due to the development of thoracic aortic aneurysm (TAA) [170]; and cardiovascular calcification caused by transformed VSMCs which secrete mineralizing extracellular vesicles that form microcalcifications [171]. Here, ELN is linked to congenital heart malformation.