While the pathogenesis of NODAT associated with hepatitis C virus (HCV) infection is not yet fully understood, it is believed that direct liver cell damage, viral replication in pancreatic beta-cells (leading to their dysfunction and destruction), and the potential effect on the insulin signaling pathway (which affects the synthesis of insulin-related proteins) all play significant roles in the development of insulin resistance, impaired insulin utilization, and insufficient insulin synthesis and secretion [30]. This evidence concerns the gene INS and Insulin resistance.