That is because infections can lead to poor outcome after stroke via many different mechanisms, which may include (1) increased BBB disruption and tissue damage by neutrophil-derived various proteases, reactive oxygen species (ROS), as well as numerous inflammatory mediators; (2) impaired tissue reperfusion through endothelia-dependent mechanisms; (3) increased platelet activation and microvascular coagulation; and (4) CRP-induced ischemic tissue injury via a complement-dependent mechanism [15, 16]. The gene discussed is CRP; the disease is Stroke.