Support for this proposal comes from a mouse model of type 1 diabetes with an activated ER stress response that inhibits ATF4 activity; these mice show a marked attenuation of the high–glucose-induced production of Intercellular Adhesion Molecule (iCAM), Tumor necrosis factor (TNFa), and vascular endothelial growth factor (VEGF) and a significant overall amelioration of retinal inflammation (Chen et al., 2012). Here, VEGFA is linked to type 1 diabetes mellitus.