C3 is the converging point of all three complement pathways (classical, lectin, and alternative), and its cleavage product, C3a, is rapidly generated post-stroke, exerting potent pro-inflammatory and chemoattractant effects via C3aR, which is expressed on microglia, astrocytes, neurons, and endothelial cells [20,24]. This evidence concerns the gene C3 and stroke disorder.