In summary, we propose that during AMD-associated inflammation, two influencing factors need tobe considered: (i) the release of 10–100 μm bioavailable zinc will affect theoligomerization and activity of FH (31); (ii) if zincconcentrations increase even further, C3b will also form oligomers, but more importantly any C3b-FHcomplexes that are formed in Bruch's membrane will precipitate in >100 μmzinc. Here, C3 is linked to age-related macular degeneration.