Namely, whether predisposition to aberrant inflammation leads to the hallmark of Alzheimer’s disease (including late onset Alzheimer’s disease), β-amyloid deposition, or if β-amyloid cannot be cleared in certain pro-inflammatory backgrounds.5 Nevertheless, there is evidence for the involvement of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling and its downstream targets as part of this inflammatory response.6 This evidence concerns the gene NFKB1 and Alzheimer disease.