The proinflammatory cytokine TNF-α activates the NF-κB signaling pathway, leading to nuclear import of p65 and binding to the p65-binding site on the miR-497 promoter, which, in turn, inhibits the transcription of miR-497, thereby upregulating the expression of SALL4 and eventually promoting EMT and the self-renewal phenotype of HCC (Figure 6G). Here, SALL4 is linked to hepatocellular carcinoma.