Kulkarni and Afshar-Kharghan control mice (Coffey et al 2007). These functional abnormalities were associated with complement deposition and altered retinal structure. Studies using factor H puriﬁed from serum and recombinant factor H showed decreased binding of the 402His variant of factor H to CRP and heparin as compared to the wild-type 402Tyr variant (Clark et al 2006; Laine et al 2007). Despite the presence of strong data linking polymorphisms in factor H to retinal damage in AMD, further animal and human studies are required before this information may be applied to clinical use. Conclusion The ﬁeld of anticomplement therapy is a rapidly-evolving one and has much potential for future beneﬁt in clinical medicine. It will arguably have the most impact in the treatment of PNH, for which anticomplement therapy has been shown to be a highly effective treatment. 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