Collectively, we favor a model in which early in infection NOD-like receptors inhibit the initial growth of S. flexneri in the epithelial cell layer, but at later times (following the recruitment of IFNγ-producing NK cells and IFNγ secretion at the site of infection) RIG-I becomes a crucial component in the ability of the host to clear S. flexneri infection. Here, RIGI is linked to infection.