Targeting prostanoid biosynthesis with COX-2 inhibitors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), the classical pain medications, or the novel COX-2 selective inhibitors (e.g., celecoxib or rofecoxib), has been shown to reduce edema, neuroinflammation, and infarct size in rodent stroke models [153]. This evidence concerns the gene PTGER2 and stroke disorder.