IGF-1R is overexpressed in vitro and in animal models of HCC [26,36,37], suggesting that activation of the IGF/IGF-1R axis and its related signaling pathways, such as the PI3K/Akt signaling pathway, significantly contribute to the stimulation of HCC cell growth and liver carcinogenesis, especially in the presence of metabolic disorders. This evidence concerns the gene IGF1R and metabolic disease.