While the immune deficiency of Nfkb1−/− mice likely contributes to early aging, the observation that loss of Nfkb1 leads to decreased apoptosis, increased γH2AX focus formation and increased senescence not only in tissues but also in cultured cells, suggests that age-related findings with loss of this subunit are at least in part cell autonomous. The gene discussed is NFKB1; the disease is Immunodeficiency.