In hepatocellular carcinoma (HCC) cells that heavily express c-MET, hepatocyte growth factor (HGF) activated the downstream PI3K/Akt and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathways through c-MET and concurrently reduced the anticancer effects of lenvatinib (a tyrosine kinase inhibitor) and promoted EMT [41]. Here, MET is linked to hepatocellular carcinoma.