One explanation is that IFNγ-dependent control of S. flexneri occurs in non-myeloid cells (such as epithelial cells) early during infection, while at later timepoints IFNγ-activated macrophages dominate the IFNγ-dependent response; consistent with this hypothesis, we found that neither RIG-I nor MAVS is important for IFNγ-dependent killing of S. flexneri in primary macrophages (Fig. S2). The gene discussed is RIGI; the disease is infection.