Considering that activators of the NF-κB signaling pathway are determinants of inflammation and aging process (Balistreri et al., 2013) and that CNS inflammation is present in the early stages of age-related disorders such as AD but disappears with disease progression (Streit et al., 2009), our in vitro aged microglia may represent a dystrophic and irresponsive phenotype whose functions have progressively declined as recently observed in mice with AD-like pathology (Krabbe et al., 2013). The gene discussed is NFKB1; the disease is Alzheimer disease.