Whereas complement activation, and C3a in particular, can contribute to endothelial cell activation, inflammatory cell recruitment and tissue injury in the acute phase after cerebral ischemia, C3a-C3aR signaling evidently also supports functional recovery by stimulating post-stroke neural plasticity including cell replacement, reorganization of axonal circuitry, and synaptogenesis. This evidence concerns the gene C3AR1 and brain ischemia.