Following an ischemic stroke, a robust inflammatory response occurs, leading to the rapid recruitment of neutrophils.[23] These neutrophils release NETs, which contain a large number of pro‐inflammatory factors and exacerbate nerve damage.[9] Intracellular ROS is known to prompt the release of granular proteins, like myeloperoxidase (MPO) and neutrophil elastase (NE), as well as histone H3 citcitylation (H3Cit), all of which are essential for NETs formation (Figure4A).[24] Therefore, we assessed APTS's ability to scavenge ROS. This evidence concerns the gene ELANE and ischemic stroke.