Statins lower plasma lipid levels by inhibiting HMG CoA reductase, the enzyme responsible for converting HMG CoA to mevalonate, a rate-limiting step in cholesterol biosynthesis. Multiple observational studies have suggested that statins may be of benefit in patients with a variety of severe infections [17] [18] [19] [20] [21] [22] by exerting an effect in attenuating inflammation [23, 24] . The mechanism of this activity is uncertain but may involve their ability to restrict cholesterol availability in cell membranes of the innate immune system. Cholesterol is a key component of lipid rafts, membrane-associated microdomains that support cell signaling in response to exogenous inflammatory stimuli. Raft disruption may attenuate the cellular response to inflammatory stimuli [25, 26] .