While it remains possible that FlaA produced by MogR-negative bacteria inappropriately activates TLR5 signaling [2], this hypothesis seems less likely given that MogR-negative bacteria cultured at 37 °C prior to infection, a condition where FlaA levels are dramatically reduced, still exhibited a 10-fold virulence defect and an approximately 20% intracellular spreading (plaquing) defect (Table 1). The gene discussed is TLR5; the disease is infection.