It is possible that in young ECM, awash with potential FH/FHL-1 anchoring partners, the Y402H polymorphism is well tolerated, and that the age-related decrease in these GAGs leads to less FH/FHL-1 binding and an increase in complement turnover and immune cell recruitment into the choroidal space: both hallmark features of AMD. This evidence concerns the gene FHL1 and age-related macular degeneration.