MET and neoplasm: hHGF knock-in H596 models exhibit rapid tumor growth and constitutive tumor EMT due to hHGF secretion by mouse stromal cells, thereby enhancing tumor HGF/MET signaling [11]; H596 tumors are particularly receptive to enhanced HGF secretion due to the presence of a MET exon 14−skipping mutation that suppresses proteasome-mediated MET degradation [12].