As one of the terminal mediators of the complement system, genetic depletion or a specific antagonist of C3aR was used to define the role of C3aR and modulate its activity during different kinds of diseases, including intestinal ischemia/reperfusion injury, myocardial ischemia and reperfusion injury, hypertension, brain death induced by lung injury, kidney disease, type 2 diabetic nephropathy, arthritis, AD, intracerebral hemorrhage, and ischemic stroke [34, 67, 172, 174, 339, 405-413]. This evidence concerns the gene C3AR1 and ischemic stroke.