In a study set out to define the spectrum and mechanism of HGF/MET-mediated resistance, it was noted that HGF-induced EGFR TK inhibition is a very common mechanism in human cancers and in such cases the kinase-inactive EGFR directly interacts with and stabilizes several cancer-relevant proteins, including AXL, EphA2 and the Cub domain containing protein 1. This evidence concerns the gene CDCP1 and cancer.