NFKB1 and cancer: Next to TLRs, also the major Hp cytotoxin CagA can directly utilize NFκB and STAT3, in either a phosphorylation-dependent or phosphorylation-independent manner [124, 125] or through the interaction with TNF receptor–associated factor 6 (TRAF6) and TGF-β-activating kinase 1 (TAK1) [19, 25, 64], leading to the transformation from chronic inflammation to cancer [113, 124, 125].