Studies in vitro have suggested that interference with type I interferon (IFN) signaling through the Toll-like receptor 3 (32) and IRF-7 (33) are mechanisms by which EV-D68 evades the host innate immune response, but this has yet to be confirmed in vivo. In the lung, the early proinflammatory cytokine and chemokine response to EV-D68 infection has been characterized in both mice (34) and cotton rats (35), prompting the recruitment of inflammatory cells; however, the relevance of specific pathways and cell types to EV-D68 clearance is unknown. The gene discussed is IFNA1; the disease is infection.