In a DEN/CCL4-induced HCC mouse model, SALL4 directly modulates the expression of miR-146a-5p by binding to its promoter, and blocking the SALL4/miR-146a-5p interaction in HCC downregulates the expression of inhibitory receptors on T cells, reverses T-cell exhaustion, and delays HCC progression (Yin et al. 2019). This evidence concerns the gene SALL4 and hepatocellular carcinoma.