Our results lay a foundation for a follow up cohort study with larger sample size and including diabetic and non-diabetic CHC patients with and without fibrosis that would have value to illustrate the role of IR as a separate metabolic factor for HCC development and enable investigation of the role of other individual metabolic signals such as adiponectin, and leptin which may have particular involvement in hepatocarcinogenesis in patients infected with HCV-4. This evidence concerns the gene LEP and cryohydrocytosis.