Neutrophils, as key effectors of innate immunity, play a pivotal role in post-stroke inflammation by releasing reactive oxygen species (ROS), matrix metalloproteinase-9 (MMP-9), and neutrophil extracellular traps (NETs), thereby exacerbating blood-brain barrier disruption, cerebral edema, and atherosclerotic plaque instability (Tang et al., 2024). This evidence concerns the gene MMP9 and Stroke.