Hypoxia, as well as hyperactivity of the complement system, together with the inflammatory process, leads to disturbances in the pro/antiangiogenic balance and RPE cells overexpression of proangiogenic vascular endothelial growth factor (VEGF), which plays a key role in the pathogenesis of CNV/AMD [1, 4]. The gene discussed is VEGFA; the disease is age-related macular degeneration.