In addition to the potential metabolic benefits, the impact of such therapy on the liver fibrosis might also be in the focus of interest especially because the Fibroblast Activation Protein which is a duplicate molecule of DPP-4 (FAP-DPP-4 shows 88% homology at cDNA level) is present at the tissue remodeling interface on hepatic stellate cells (HSCs, ITO cells) which are thought to primarily produce the accumulating extracellular matrix (ECM) proteins (including collagens) in chronic liver diseases eventually leading to the fibrosis and cirrhosis of the liver.[23]. Here, FAP is linked to fibrosis.