As described in detail already, this polymorphism affects the coding sequence of CCP7 in the full-length FH protein and FHL-1, since they are both produced by alternative splicing of the CFH gene; the altered specificity for GAGs (e.g., in the human Bruch’s membrane) as well as changes to other binding functions (e.g., CRP and apoptotic/necrotic cells) are of likely relevance to the pathology of AMD, where local (chronic) inflammation, driven by complement dysregulation, is thought to be of central importance [30, 31, 174]. The gene discussed is FHL1; the disease is age-related macular degeneration.