NFKB1 and hepatocellular carcinoma: Because the membrane-bound TLRs share many properties and similar activation mechanisms, we assume that the occurrence and progression of HCC lead to increased translocation or recruitment of all MyD88-dependent TLRs into lipid rafts, which results in the constitutive activation of NFκB to produce augmented proinflammatory cytokines and promote cell proliferation and survival.