XIAP and Sepsis: Besides, we provided some valuable evidence, for example, P2X7R activates brain cells to produce a lot of ROS in vivo sepsis, mediates mitochondrial damage and Omi/HtrA2 translocation from mitochondria to cytoplasm, thereby promoting the cleavage of the intracellular apoptosis-inhibiting protein XIAP through Omi/HtrA2, and increases the expression of proapoptotic protein such as cleaved-Caspase-3 (Figure 6), ultimately leading to cognitive impairment.