Likewise, MET variants with activating mutations in the kinase domain could also require ligand stimulation to achieve full receptor activation, as suggested by numerous experimental observations demonstrating that most of the kinase-domain-mutated MET forms recorded in renal cancers can be further stimulated by HGF, with the exception of the form bearing the M1268T mutation (Chiara et al., 2003; Graveel et al., 2004; Michieli et al., 1999; Graveel et al., 2005). This evidence concerns the gene MET and renal carcinoma.