In the retinas of diabetic retinopathy patients and mouse model, the expression and enzymatic activity of Adam17 are upregulated, with its chemokines substrates such as CXCL16 and CX3CL1 [83, 84], and inactivation of endothelial Adam17 or its genetic inhibitor, the tissue inhibitor of matrix metalloproteinases-3 (TIMP3) ameliorates pathogenesis both in diabetic retinopathy and retinal ischemia reperfusion [83, 85–87], indicating an important role of Adam17 in vascular ocular pathologies. This evidence concerns the gene TIMP3 and diabetic retinopathy.