Although the impact of astroglial inactivation of NF-κB has not been established in AD mouse models, recent evidence demonstrates that blockage of NF-κB transcriptional activity in astrocytes can extensively reduce inflammation and improve recovery, thus suggesting that inhibition of NF-κB in astrocytes may be regarded as a potential therapy for AD (Medeiros and LaFerla, 2013). Here, NFKB1 is linked to Alzheimer disease.