NOX2 exacerbates acute brain injury after stroke by activating the NLRP3 inflammasome and blocking angiogenesis through the excessive production of ROS followed by excessive autophagy activation, but it repairs the brain during the delayed stage by generating a small quantity of ROS, inhibiting the NLRP3 inflammasome and triggering angiogenesis via a low level of autophagy activation, which is associated with the PI3K/Akt/NF-kB signaling pathway (Fig. 10). The gene discussed is NFKB1; the disease is stroke disorder.