While type I IFN signalling has been shown to be critical for antiviral responses following infection with two human H5N1 isolates [54], a lack of IL-1R, IL-6, macrophage inflammatory proteins-1α (MIP-1α/CCL3) or TNF receptor 1 (TNFR1) had limited or no impact [55], suggesting that individual cytokines or pathways do not mediate severe H5N1 disease. The gene discussed is CCL3; the disease is infection.