2–5OAS proteins are stimulated by IFNs to synthesize 2-5A oligoadenylates that activate RNaseL to cleave dsRNA [27,28]; amazingly, the response of CHC patients to IFN-based treatment is related to RNaseL and it has been described that NS5a can inhibit IFN signaling through its direct binding to 2–5OAS [29]. The gene discussed is IFNA1; the disease is cryohydrocytosis.