In comparison, both Ifnar1-/- and Stat1-/- mice showed extensive WNV antigen staining in the myenteric plexus, the lamina propria, and enterocyte layers, with greater infection in the duodenum than other intestinal segments (Fig. 2a and Supplementary Fig 1b); as the enterocyte infection phenotype appeared more prominent in Stat1-/- than Ifnar1-/- mice, signaling from IFN-λ, IFN-γ, or other cytokines upstream of STAT1 signaling might still contribute to control of WNV infection in the GI tract, particularly in the absence of type I IFN signaling. The gene discussed is STAT1; the disease is infection.