Previous evidences also indicated that pathological phenotype modulation of VSMCs plays an important part in the growth of many different types of cardiovascular diseases such as postangioplasty restenosis, atherosclerosis, and hypertension, and GAX maintains VSMCs contractile phenotype and monitors VSMCs proliferation and migration by targeting the Rap1A gene.[24] Our study indicated that expressions of ET-1 and VEGF were negatively correlated with the expression of GAX, whereas expressions of NO and SOD were positively correlated with GAX expression. The gene discussed is SOD1; the disease is atherosclerosis.