Although the expression of C3aR in the brain is not limited to astrocytes and the positive effects of C3a on post-stroke recovery conceivably involve also direct modulation of the functions of neurons and microglia, the increased expression of Igf1 and Thbs4 in the peri-infarct cortex of C3a-treated mice points to IGF-1 and THBS4 as glia-derived mediators of the effects of C3a/C3aR signaling on neuronal connectivity after stroke. The gene discussed is THBS4; the disease is Stroke.