MET and neoplasm: A study by Finisguerra et al. suggested that neutrophils with antitumour capacity were dependent on MET/HGF pathway, with their consequent detrimental depletion by treatments with MET inhibitors.54 The proposed model however, based on mice reconstituted with upfront MET-deficient hematopoietic cells, did not allow the exploration of myeloid elements within the tumour microenvironment with potentially immune-suppressive functions.