In majority types of cancers, MET is transcriptionally modulated by intratumoral hypoxia, ligand-independent activation or increased susceptibility to HGF 9, and antagonized by some molecules such as interferon-induced protein 44-like (IFI44L) and angiopoietin-like protein 1 (ANGPTL1) 10, 11. This evidence concerns the gene HGF and cancer.