Evidence from studies in humans and experimental animals suggests that inflammation is a key mechanism in formation and rupture of cerebral aneurysms.1–10 Several inflammatory mediators, including cyclooxygenase‐2 (COX‐2) and microsomal prostaglandin E2 synthase‐1 (mPGES‐1), are upregulated in the walls of cerebral aneurysms.3 We have demonstrated recently that COX‐2 and mPGES‐1 are expressed in the walls of human cerebral aneurysms.11 These inflammatory molecules were more abundantly expressed in ruptured than in unruptured aneurysms.11 This evidence concerns the gene PTGES and brain aneurysm.