Studies in Tg2576 transgenic mice models of AD, macrophage inflammatory protein-1α (MIP-1α−/−), and CC-chemokine receptor 5 (CCR5−/−)-deficient mice demonstrated that a subsequent NF-κB and mitogen-activated protein kinase (MAPK) pathways trigger a shift from the anti-inflammatory to pro-inflammatory phenotypes in astrocytes and microglia. The gene discussed is NFKB1; the disease is Alzheimer disease.