For a number of years, immunologists have strived to understand the mechanisms associated with treatment-induced eradication of hepatitis C virus (HCV). However, interferon (IFN)-α–based therapies did not allow studies examining the role of the virus itself on innate and adaptive immunity to HCV. The study by Serti et al1 published in this issue of Gastroenterology provides a unique opportunity to assess the effect of virus on innate immunity, particularly natural killer (NK) cells, which were previously described by the same authors and other groups to be dysfunctional in this setting (reviewed by Golden-Mason and Rosen2).