The involvement of the ECM in the pathogenesis of AMD is further supported by additional AMD risk genes such as TIMP3 (tissue inhibitor of metalloproteinases-3), which inhibits MMPs (matrix metalloproteinases) and is involved in degradation of the ECM [22], and ARMS2, which interacts with several ECM proteins [23]. The gene discussed is TIMP3; the disease is age-related macular degeneration.