There is ample evidence that the RPE BrM/choriocapillaris complex is involved in AMD pathogenesis, but immunohistochemical studies of TCC/MAC deposition in human eye tissue provide evidence that the main site of complement activation is the choriocapillaris layer and not the RPE (2, 7, 9, 10), suggesting that BrM acts as a barrier to complement proteins and therefore complement activation. This evidence concerns the gene VTN and age-related macular degeneration.