We also found increased mRNA expression of the TGFβ receptor 2 (TGFBR2), of the matrix metalloprotease ADAMTS6, known to be up regulated in ARPE-19 cells upon TNFα stimulation [13] and CTGF, as well as decreased expression of TIMP3, recently established as a signature gene of potential role in AMD pathogenesis [14] all consistent with enhanced tissue remodeling capacity important for lesion repairing. The gene discussed is TNF; the disease is age-related macular degeneration.