Previous studies have reported on the inflammatory changes and elevation of vascular degradation molecules in unruptured and ruptured intracranial aneurysms (IAs) [2, 3], and studies using animal models have indicated the possibility of developing treatments using a mineralocorticoid receptor (MR) blocker and an angiotensin type I receptor (AT1R) blockade [4, 5]. This evidence concerns the gene NR3C2 and Dilatation of the cerebral artery.