Due to their high prevalence, non-alcoholic fatty liver disease (NAFLD), insulin resistance (IR) and hepatitis C virus (HCV) infection are bound to cohabit. However, the relationship between these 3 entities is complex and multilayered. HCV, particularly genotype 3, may induce a "viral" steatosis, morphologically indistinguishable from the steatosis of NAFLD but with different implications and prognosis. On the other hand, epidemiological and experimental data show that patients with HCV have a higher risk of developing IR and, in susceptible individuals, type 2 diabetes (T2D). In patients with HCV, T2D increases fibrosis progression rate, increases the incidence of HCC, worsens liver-related outcomes and worsens response to interferon-α based therapy. We conclude by discussing a possible increased incidence of cardiovascular events in HCV patients.