Since cancer patients with increased Axl expression show disease progression and advanced tumor staging resulting in rather metastatic phenotypes [27], the hypothesis is supported that Gas6 levels are in excess compared to sAxl and free Gas6 is available to activate non-shedded Axl receptor for amplifying Gas6-dependent Axl signaling in liver fibrosis and HCC (Figure 4B, right panel). This evidence concerns the gene AXL and hepatocellular carcinoma.