Aspirin, despite its well-established role in secondary prevention, potentiates gastrointestinal mucosal injury and increases the risk of intracranial hemorrhage due to its irreversible inhibition of cyclooxygenase-1 (COX-1), which suppresses thromboxane A2 production and impairs primary hemostasis [22,23]. The gene discussed is PTGS1; the disease is intracranial hemorrhage.