Senescent cells have been shown to secrete a plethora of factors, of largely NF-κB-driven inflammatory cytokines chemokines and immune modulators and upregulate enzymes that degrade extracellular matrix, changes collectively called the senescence-associated secretory phenotype (SASP),10, 11, 12 which may, at least in some cell types, help to reinforce the senescence arrest.13, 14 Thus, although senescence functions as an antiproliferative program, capable of limiting tumorigenesis, senescent cells can also promote an inflammatory microenvironment that stimulates tumor progression. Here, NFKB1 is linked to neoplasm.