The pathophysiological rationale of Gas6/Axl deleterious role probably consists in its capacity to activate HSCs and modulate hepatocyte differentiation, as suggested by a preliminary study which demonstrated that in HCC cancer cell lines Gas6/Axl can enhance cell invasiveness through transcriptional activation of Slug which induces epithelial to mesenchymal transition (EMT) [114]. The gene discussed is GAS6; the disease is hepatocellular carcinoma.