Our findings suggest that CFH, ARMS2, IL-8, TIMP3, SLC16A8, RAD51B, VEGFA and COL8A1 may contribute to the onset of wet AMD at different levels, particularly the following: induction of angiogenesis; alteration of ECM remodeling mechanisms and of BrM integrity and permeability; modification of RPE and photoreceptor cell activities; and over-activation of inflammatory and immune responses. This evidence concerns the gene TIMP3 and wet macular degeneration.