As discovered in an in vitro study on cerebral ischemia-reperfusion injury, following cerebral ischemia-reperfusion injury, complement activation produces C5a, which interacts with C5a receptor 1 to inactivate mTOR, leading to autophagy activation through the Akt/mTOR pathway and eventually neuronal apoptosis and brain damage [19]. The gene discussed is AKT1; the disease is brain ischemia.