This hypothesis is supported by the Holstein et al. group that proposed there might be a switch predisposing liver fibrosis, cirrhosis, or even HCC development, where even in the event of a cleavage of Axl, the inhibitory Axl shedding mechanism is circumvented due to the presence of abundant nonshedded Axl receptors that will overcome the loss of proteolytically cleaved Axl. Here, AXL is linked to Hepatic fibrosis.