Activation of β-ARs reduced levels of iNOS and other inflammatory molecules, such as interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and prostaglandin E2 (PGE2) in human retinal endothelial cells, and rat Müller cells in an in vitro model of hyperglycemia [95]. This evidence concerns the gene TNF and Hyperglycemia.