Our observations suggest that sustained exposure to oxidative stress might impair RPE-derived MCP-1-mediated scavenging macrophages recruitment and phagocytosis which might lead to incomplete clearance of proinflammatory debris, infiltration of proangiogenic macrophages and ultimately to progressive drusen accumulation and CNV in smoker patients with AMD. Here, CCL2 is linked to age-related macular degeneration.