Micklish et al. suggested that the involvement of ARMS2 in the complement-mediated clearance of cellular debris by the process of opsonization of apoptotic and necrotic cells and the ARMS2 AMD risk variant increases the chance of drusen formation by the accumulation of lipoproteinaceous deposits in Bruch’s membrane [90]. The gene discussed is ARMS2; the disease is age-related macular degeneration.