Whilst mutations in the upstream activators and individual subunits of NF-κB are rare, it is far more likely that increased and even consistent NF-κB activation is promoted by inflammatory stimuli, the source of which is likely to vary widely from underlying inflammatory conditions (i.e., viral hepatitis and EBV (Epstein-Barr virus), cellular senescence and senescence associated secretory proteins and immune activation by malignant cells) [2,3]. Here, NFKB1 is linked to viral hepatitis.