NFKB1 and hepatocellular carcinoma: TIFA overexpression promotes oligomerization and poly-ubiquitinylation of TRAF6, which in turn activates TAK1 and IKK.4,5 The TAK1 and IKK activation links TRAF6 to NF-κB in the IL-1/TLR4 pathway.6 Recent studies also demonstrated that TIFA oligomerization was indispensable for innate immunity induced by bacterial metabolite HBP (heptose-1,7-bisphosphate).7,8 Our previous findings showed that: (a) TIFA expression is suppressed during HCC progression and (b) TIFA reconstitution induced the expression of p53 thereby promoting apoptosis, while suppressing proliferation among surviving cells.