IR and the binding of IGF-1 to insulin-like growth factor 1 receptor (IGF-1R) will trigger their downstream cellular pathways, such as phosphatidylinositol-3 kinase (PI3K), protein kinase B (AKT) and mitogen-activated protein kinase (MAPK), which induce HCC cells to proliferate and inhibit apoptosis, ultimately promoting the tumorigenesis of HCC (35, 36). Here, IGF1R is linked to hepatocellular carcinoma.