MET and renal carcinoma: Using c-Met mutant proteins that were found in renal cancers, Joffre et al. showed that the mutant versions of c-Met underwent an increased Cbl–Grb2-dependent recycling and a concomitant aberrant activation of GTPase Rac1, leading to enhanced cell migration, anchorage-independent cell growth and in vivo tumorigenesis [48].