Current models for AMD suggest that the accumulation of drusen, extracellular deposits located between the retinal pigment epithelium (RPE) and Bruch’s membrane, coupled with defective regulation of C3 by CFH, result in inflammation and cytolysis that disrupt the function of RPE cells and their glial-like interactions with photoreceptors (8,9). The gene discussed is CFH; the disease is age-related macular degeneration.