It has been reported that the dysfunction of the CREB signaling in AD mouse models [16,17] and regulation of the phosphorylation of CREB has shown promising rescuing effects against neuroinflammation and memory dysfunction, as the phosphorylated CREB has been suggested to inhibit the phosphorylation of NF-κB by reducing the binding of CBP to the NF-κB, where it will reduce the pro-inflammatory processes [18]. Here, NFKB1 is linked to Alzheimer disease.