A remarkable hallmark of highly virulent human pathogens is the ability, acquired through evolution, to inhibit this innate immune response by the expression of viral factors that affect one or several steps of the above described signaling cascade. Some of the most notorious examples are the influenza virus NS1 protein, that targets RIG-I for degradation, minimizing the sensing of influenza virus PAMPs by this PRR [20] or the Hepatitis C virus NS34A protease complex that cleaves the adaptor IPS-1 to interrupt the signaling that ends with the activation of IRF3, NFkB and the subsequent production of type I IFN in human hepatocytes [21] .