Importantly, nuclear factor of kappa-light-chain-enhancer of activated B cells (NF-κB) hyperactivation due to inhibitor of κB kinase (IKK) knockout (KO) results in complement expression by astrocytes because C3 protein secretion is driven by NF-κB activation in these cells, and such responses worsen Aβ-associated pathology, with reduced numbers of synapses and shortened dendritic lengths, and impaired synaptic functions, due to reduced microglial Aβ phagocytosis in AD mouse models (42, 43). The gene discussed is NFKB1; the disease is Alzheimer disease.