C3 deficiency and pre-treatment of mice with C3aR antagonist reduced granulocyte infiltration, infarct volume and neurological deficit scores assessed 24 h after transient cerebral ischemia [63], and mice that were treated with SB290157, a C3aR antagonist [68], starting before the induction of transient ischemia developed smaller infarcts as assessed 7 days after ischemia [69]. Here, C3 is linked to ischemia.