MET and neoplasm: High level of HGF in the tumour microenvironment favouring paracrine tumour-stroma crosstalk, c-Met overexpression, ligand-independent activation, exon 14 deletion and less often kinase domain mutations are well documented mechanisms utilised by the tumour cells (Comoglio et al., 2018; Baldacci et al., 2018; Duplaquet et al., 2018).