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. Here, TIFA is linked to hepatocellular carcinoma.