Furthermore, based on in vivo and in vitro subarachnoid hemorrhage (SAH) models, Zhang et al. demonstrated that TLR4 plays a crucial role in mediating neuroinflammation caused by insults resulting from SAH, while MyD88 and NF-κB act downstream, and the neuroprotective effect of ATX primarily relies on inhibiting the TLR4 signaling pathway and the subsequent proinflammatory response36. This evidence concerns the gene NFKB1 and subarachnoid hemorrhage.