The cellular source of iNOS/NO following influenza infection in mice was shown to be CCR2+ inflammatory monocytes that accumulate in the lungs: CCR2−/− mice survived a lethal challenge of influenza infection (PR/8/34 strain) and had significantly reduced accumulation of iNOS-expressing macrophages in the lung, with no associated increase in viral titers or dissemination (53). The gene discussed is CCR2; the disease is influenza.