Control of choroid neovascularization may be important but insufficient to preserve long-term vision threatened by age-related macular degeneration. A retrospective analysis of patients who were early participants in anti-vascular endothelial growth factor studies, other pathologic processes, particularly fibrosis and atrophy, have participated in vision loss independent of new vessel growth. The recent interest in combination treatment strategies has been dominated by more effective blockade of angiogenic signaling, but it may also be necessary to incorporate therapies that block fibrosis, inhibit atrophy or other pathophysiologic processes not directly related to neovascularization to achieve the ultimate goal of preserving sight for a long term.