Influenza researchers have embraced the cytokine storm mechanism as an explanation for the fatal human disease caused by avian H5N1 influenza (7) (8) (9) . Likewise, the pandemic influenza outbreak of 1918 is likely to have induced an overwhelming and fatal cytokine response in humans, as mice and monkeys infected with a reconstructed 1918 influenza virus exhibited a dysregulated immune response and hypercytokinemia, which leads to death (10) (11) (12) . The inevitable 3-6-month delay in vaccine availability in the event of a pandemic (13) means that treatments to prevent death (but not necessarily infection) are a necessity. Existing problems with antiviral drugs (stockpiles not big enough to treat populations, drugs need to be taken prophylactically or very soon after infection, resistant virus strains have emerged) further necessitate investigation into other treatments (14) . Targeting the detrimental host response generated by particularly pathogenic strains of influenza virus would allow disease severity to be reduced to the point where people will be sick, but will not die as a result of infection. We see agents with an ability to damp inflammatory cytokine release [be they natural or pharmaceutical (15) ] as ideal candidates for influenza disease treatments, particularly during the period while a new vaccine is being generated, and as useful adjunct treatments to antivirals. As has been suggested for statins (16) , using agents that are in use in the human population for the treatment of other conditions means that the safety of such agents is already established, as is the optimal human dose range.