More recently, a study shows that the deletion of superoxide generating NADPH oxidase 2 (NOX2) reduces the expression of NLRP3 in a traumatic brain injury model, and it disturbs the NLRP3-TXNIP interaction in the cerebral cortex of mice after ischemic stroke, but not in the umbilical vein endothelium, which suggests a tissue-specific role of cytosolic ROS in NLRP3 inflammasome activation [95]. Here, NLRP3 is linked to ischemic stroke.