Moreover, the increased level of either endogenous or exogenous GSTA2 protein could activate the expression of several EMT-promoting proteins including N-cadherin, vimentin, and claudin-1, while suppression of GSTA2 in the metastatic HCC cell line could inhibit its in vitro and in vivo metastatic ability. Here, GSTA2 is linked to hepatocellular carcinoma.