They proved that TLR4 expression increased in mice with AD, and inhibition of TLR4 triggered microglia from an inflammatory M1 phenotype to a protective M2 phenotype and protected neurons from cytotoxicity of activated BV2 microglia by downregulating MyD88/NF-κB and NLRP3 signaling pathways in AD [33]. The gene discussed is NFKB1; the disease is Alzheimer disease.