In view of the complex effect of genetic polymorphisms on ischemic stroke progression, the lack of an association between CYP11B2 polymorphism and ischemic stroke susceptibility may attribute to other polymorphisms in RAAS (angiotensinogen T174M and M235T, angiotensin-converting enzyme I/D and 4656 2/3CT repeat, angiotensin II type 1 receptors A1166C and A153G, chymase G1903A), which could affect the expression of aldosterone and cerebrovascular disease susceptibility [1], [29], [30]. The gene discussed is CMA1; the disease is ischemic stroke.