Furthermore, during pneumonia, lung neutrophils increased expression of a number of IFN-responsive genes, including the inflammatory mediators Ccl2, Ccl5, and Cxcl10, antiviral effector enzymes Oas1, Oas2, Oas3, and Ddx60, and transcription factors and signaling molecules involved in the interferon pathway such as Irf1 and Stat1 (Supplementary Table 1). The gene discussed is OAS1; the disease is pneumonia.