MET and neoplasm: In summary, our preclinical studies have shown that gene amplification, but not gene mutation, confers “oncogenic driver” potential on MET. Tumor cells positive for MET amplification are thus dependent on (“addicted to”) sustained MET activity for their growth and survival, with the result that inhibition of MET signaling either with a small-molecule MET inhibitor or by RNA interference targeted to MET mRNA has marked antitumor effects both in vitro and in vivo.