Extracellular HMGB1 and its receptors, RAGE, TLR2, and TLR4, have been implicated in mechanisms of many inflammatory diseases, including sepsis, atherosclerosis, and rheumatoid arthritis (144) by induction of senescence-associated secretory phenotype via NF-kB activation (145). Here, NFKB1 is linked to atherosclerosis.