Our peptide is based on studies by Zou and colleagues, who found that a YLGA amino-acid motif located near the extracellular N terminus of the alpha-subunit of the Met oncogene is necessary and sufficient to specifically bind the extracellular portion of Fas and to act as a potent FasL antagonist and inhibitor of Fas trimerization in a mouse model of fatty liver disease [42]. Here, FAS is linked to fatty liver disease.