Disruption of the acetylation/deacetylation balance may lead to sustained transcription of pro-inflammatory genes controlled by NF-kB and AP-1, resulting in increased influx of activated microglia/macrophages to already inflamed tissue and potentially creating the chronic cycle of inflammation that is the hallmark of neurodegenerative diseases [62]. This evidence concerns the gene NFKB1 and neurodegenerative disease.