To assess whether SLAMF8’s role in AD is mediated through TLR4/NF-κB activation, we treated Aβ1−42-exposed SH-SY5Y cells and LPS-stimulated HMC3 cells, with and without SLAMF8 overexpression, with TAK-242, a selective TLR4 inhibitor that blocks NF-κB activation. This evidence concerns the gene NFKB1 and Alzheimer disease.