Further support comes from a previous study showing that in AD the brain contains increased levels of BACE1, C99 and NF-κB, and NF-κB expression leads to increase of BACE1 promoter activity and BACE1 transcription, while knockout of NF-κB decreases BACE1 gene expression in LPS-injected mice [6]. The gene discussed is NFKB1; the disease is Alzheimer disease.