SALL4 and hepatocellular carcinoma: A study with hepatocellular carcinoma (HCC)-derived EV indicated that miRNA-146a 5p from EV contributed to M2-like macrophage polarization, and that the suppression of Sal-like protein (SALL)4, a transcription factor for miRNA-146-5p, reversed T cell exhaustion induced by these macrophages in vivo [99].