In addition to the pro-oncogenic risk resulting from the development of nonalcoholic steatohepatitis (NASH) and metabolic cirrhosis, obesity may favor HCC occurrence even in absence of significant liver fibrosis by promoting systemic and hepatic inflammation, inducing oxidative stress and lipotoxicity, stimulating the insulin-like growth factor-1 (IGF-1) axis by hyperinsulinemia, and favoring hormonal changes [141]. The gene discussed is IGF1; the disease is obesity due to melanocortin 4 receptor deficiency.