Mechanistically, the anti-neuroinflammatory effects of SAD in ischemic stroke may be attributed to its inhibitory action on high mobility group box 1 (HMGB1) nuclear-to-cytoplasmic translocation and subsequent blockade of the TLR4/MyD88/NF-κB signaling cascade activation (Zhang et al., 2020). The gene discussed is TLR4; the disease is ischemic stroke.