Mechanistically, elevated c-Met transcription and overexpression of c-Met are associated with dysregulation of downstream signaling cascades (i.e., STAT3, MEK, and PI3K-AKT), MET missense mutations and MET splicing, promoting HCC cell metabolism and biogenesis, or driving tumor-initiating stem-like cell phenotype (28–30). This evidence concerns the gene MET and hepatocellular carcinoma.