Because metabolic abnormalities caused by metabolic syndrome have a great impact on liver carcinogenesis, we considered the possibility that metabolic disorders, such as insulin resistance and activation of the IGF/IGF-1R axis, might be effective targets in the prevention of HCC, and we tested this using animal models of obesity- and diabetes-related liver carcinogenesis. Here, IGF1R is linked to obesity due to melanocortin 4 receptor deficiency.