In addition to the oxidative stress hypothesis, the β-amyloid (Aβ) cascade hypothesis, and the tau protein phosphorylation hypothesis, there is increasing evidence suggesting that the neuroinflammation hypothesis is also an important factor in the pathogenesis pathway of AD, in which the TLR4/NFκB/NLRP3 inflammatory pathway, as a classical neuroinflammatory pathway, has received increasing attention in the study of AD pathogenesis. This evidence concerns the gene NFKB1 and Alzheimer disease.