The familial TAA is predominantly caused by genomic alteration that encodes extracellular matrix proteins and stimulates TGF-β signaling pathway, while the sporadic TAA presented with increased inflammation and vascular degradation (63, 64).In addition, another fatal vessel vascular disease aortic dissection (AD) also presented with inflammation and structural destroy, wherein macrophages are the hub of inflammation in the aortic wall and angiotensin II (Ang II) has been shown to be an important factor for macrophages stimulation (65, 66). The gene discussed is AGT; the disease is Aortic dissection.