HGF makes the cancer cells independent of EGFR signaling and enables EGFR to interact with other proteins such as CUB domain-containing protein-1 (CDCP1), EphA2 and AXL, forming a c-Met (HGFR)-EGFR cross-talk that can't be inhibited by EGFR TKI treatment [546]. This evidence concerns the gene EGFR and cancer.