Interestingly, increased cell surface availability of Axl through reduced receptor proteolysis and shedding has been described as a resistance mechanism to MAPK-signalling inhibitors and might account for the worse survival figures seen during sorafenib treatment.55 Our results suggest that Axl is a putative therapeutic target expressed in primary and metastatic HCC and that its inhibition influences the sensitivity of HCC cells to sorafenib and reverts the hypermotile phenotype that accompanies adaptive drug resistance.23 Here, AXL is linked to hepatocellular carcinoma.