Since a similar NS3 protease/NS5A inhibitor DAA combination failed to clear HCV genotype 2a and 2b infection in an HCV animal model in vivo[60] and viral resistance has been observed for DAAs in particular for genotype 2 and 3 in randomized clinical trials (for review see [26]), our data suggest that the antiviral strategy described in this study may address limitations of DAAs in particular for non-genotype 1 infections. This evidence concerns the gene KRAS and infection.