In conclusion, we demonstrated that (a) human activated HSCs can express and release galectin-1, (b) HSC-derived galectin-1 promotes HSC-induced T cell apoptosis and Th1/Th2 cytokine balance skewing, (c) HSC-derived galectin-1 promotes HCC progression by improving immune privilege, and (d) all aforementioned effects can be inhibited by miR-22. The gene discussed is LGALS1; the disease is hepatocellular carcinoma.