In the absence of any known endogenous GrB inhibitor, the unrestrained cleavage activity of extracellular GrB in the chorio-retinal space may be central to the potential contributions of GrB to CNV in AMD pathophysiology through remodelling of the local ECM, leading to increasing pro-inflammaotry cytokine expression and release of pro-angiogenetic factors such as VEGF from the ECM. This evidence concerns the gene VEGFA and age-related macular degeneration.