Why these two regions of FH should be tuned to interacting with different GAG structures is not understood, but it does provide an explanation for why coding changes in CCPs 6–8 and CCPs 19–20 (that affect GAG binding), via mutations/polymorphisms in the CFH gene, are differentially associated as risk factors for AMD and aHUS, which are diseases of the eye and kidney, respectively [31, 49]. The gene discussed is FH; the disease is atypical hemolytic-uremic syndrome.