The pathogenesis of cerebral infarction is a subject of ongoing research, which has focused largely on two areas: first, the dysregulation of the coagulation and fibrinolysis [35, 36], not only systemically but also locally [37, 38], as exemplified by the upregulation of plasminogen activator inhibitor-1 and elevated levels of prothrombin fragments F1 and −2 and soluble tissue factor in the CSF of patients with pneumococcal meningitis [36]; and second, endothelial cell dysfunction, which may lead to localized swelling and release of pro-coagulant factors and proinflammatory cytokines [39–41]. The gene discussed is F2; the disease is pneumococcal meningitis.