Here, we investigated LUM expression in the aortic wall and serum from patients with AAD and examined the underlying molecular mechanism by using an AD mouse models including Lum-KO (Lum−/−) mice and wild type (WT) mice manifesting pathogenesis due to internal elastic lamina degeneration and hypertension via administration of β-aminopropionitrile (BAPN) and angiotensin II (Ang II), respectively. The gene discussed is LUM; the disease is Hypertension.