A study investigating the regulatory network between host factors and T cell exhaustion in HBV-related hepatocellular carcinoma revealed an HBV/pSTAT3/SALL4/miR-200c axis regulated PD-L1 expression and confirmed that miR-200c functions as a therapeutic target to reverse T cell exhaustion during HCC progression (72). This evidence concerns the gene SALL4 and hepatocellular carcinoma.