This is geographic atrophy, a world where damage to the retina is irreversibly etched into the landscape. In this advanced form of dry age-related macular degeneration, atrophic lesions form on the macula, causing loss of functional vision as they spread. To uncover what’s behind this destruction, our attention turns to the area outside the lesion, as we immerse ourselves in the little-known land of the pre-lesion where there’s still time to intervene. Below the surface, damage to the retina hasn’t yet started, but it's far from quiet. This swarming pack of proteins is called the complement system. Normally, they defend against pathogens and remove abnormal cells. Yet in geographic atrophy, or GA, too much complement activity can be insidious—in the lesion itself, but more surprisingly, in the pre-lesion where it hides unseen. This excessive complement activity depends on the leader of the pack: C3. Complement activation causes C3 to cleave, splitting it apart into the active fragments, C3a and C3b. Over by this photoreceptor, a flock of C3a’s have begun to swarm. Too much C3a can trigger chronic inflammation of the macula and cause some unwanted attention. Here, a pack of C3b’s are on the prowl, accumulating on cell surfaces, “tagging” them for phagocytosis by immune cells. What a display. But the hunt is far from over for C3b, who’s quite the busy bee—causing a subset of downstream components of the complement system to work together and form something new: the membrane attack complex, that latches onto and forms an opening in the cellular membranes of retinal pigment epithelial cells, or RPE, as well as photoreceptors. This is what can happen in the eye when the complement system becomes overactive. Seemingly healthy retinal cells die off, and the lesion continues its spread. So, our scientific exploration has shifted to the area called the pre-lesion. It’s where millions living with GA have the most to save.