Notably, the subsequent association of common and rare alleles at or near several additional complement genes (CFH, C2/CFB, C3, CFI, and C9) has had a significant impact of the formation of pathomechanistic hypotheses, with the cumulative evidence both from human genetics but also from histopathological studies highlighting a major role of the alternative complement pathway as a driver of AMD [9–21]. The gene discussed is CFI; the disease is age-related macular degeneration.