Researchers at INSERM have identified iron accumulation as a key driver of retinal cell death in dry age-related macular degeneration (AMD), opening potential therapeutic pathways for a condition with no current treatments. Their work demonstrates that excess iron triggers oxidative damage in retinal pigment epithelium cells, suggesting iron chelation could slow disease progression. This finding addresses a critical unmet need, as dry AMD affects millions worldwide and leads to irreversible central vision loss, unlike the wet form which has established anti-VEGF therapies. The iron hypothesis builds on decades of research linking oxidative stress to retinal aging, but represents the first targeted approach to interrupt this specific mechanism. Previous antioxidant trials in AMD showed modest or inconsistent results, possibly because they addressed downstream effects rather than upstream iron-mediated damage. If validated in clinical trials, iron-targeting drugs could transform treatment for the 85% of AMD patients who develop the dry form. However, systemic iron chelation carries risks including anemia, requiring careful therapeutic windows and potentially localized delivery methods to avoid compromising iron's essential cellular functions.