Experimental evidence demonstrates that in ischemic stroke models, SAA administration not only significantly reduces the expression of pro-inflammatory cytokines IL-1β and TNF-α, but also effectively suppresses the activation of key inflammatory signaling pathways including TLR2/TLR4, MyD88, and NF-κB (Ling et al., 2021; Chien et al., 2016; Zhang et al., 2018). The gene discussed is MYD88; the disease is ischemic stroke.