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. The gene discussed is C3AR1; the disease is Cerebral ischemia.