Other factors include inflammation resulting from contact of blood with foreign material; manipulation and clamping of the aorta with consequent thromboembolism; ischemia–reperfusion damage; reduced cardiac output; hemolysis with release of free hemoglobin and free iron, promoting oxidative stress [3]; contrast nephropathy in the case of recent medical imaging; downregulation of vasodilatory mediators, such as nitric oxide; and upregulation of vasoconstrictive mediators, such as endothelin, catecholamines, and angiotensin II [3]. The gene discussed is AGT; the disease is Thromboembolism.