Given the growing recognition of complement in several pathological conditions, there has been a concerted effort recently in designing therapeutics aimed at complement proteins (Ricklin and Lambris 2007) . Understanding subversion tactics of pathogens can help in designing therapeutic interventions when unwanted or runaway complement activation does more harm than good. It has been a challenge to design effective therapeutic interventions, although a number of soluble and membrane-bound complement proteins are available as potential therapeutic targets. One of the main problems is the lack of understanding of the exact molecular mechanisms involved in complement-mediated disease pathology (reviewed in Ricklin and Lambris 2007) . For instance, a good example is the use of compstatin, a synthetic compound that blocks the C3 convertase. An ideal use of compstatin would be for treatment of patients experiencing age-related macular degeneration, using intravitreal injection into the eye, much as is now done with blocking mAb to VEGF. On the other hand, systemic treatment of septic patients with compstatin runs the risk of excessive blocking of the C3 convertase, which would compromise the production of the vital opsonic factors, C3b and iC3b. Accordingly, this presents the dilemma for using complement inhibitors that target the C3 convertase. The lack of sufficient knowledge about details of complement activation (including the complement regulatory proteins) makes it difficult to predict the efficacy of complement inhibitors that would be given systemically.