The results showed that rCOMP treatment for 24 h significantly stimulated ERK and AKT phosphorylation in HCC cells in a dose-dependent manner without obvious changes of the total ERK and AKT expression levels, indicating the involvement of ERK and AKT phosphorylation in COMP-mediated promotion of migration and invasion potential of HCC cells (Fig. 5a). This evidence concerns the gene AKT1 and hepatocellular carcinoma.