My laboratory has been involved in the fields of islet transplantation and vascular complications of diabetes. Based on unexpected recent results we developed an interest in exploring a novel insulin-independent anti-diabetic function of A20/TNFAIP3, an ubiquitin-editing and NF-kB inhibitory protein that has been the focus of my lab research for the last 20 years. We ave evidence that overexpression of A20 in the liver of streptozotocin-treated diabetic mice normalizes glycemia glycemia and GTT by decreasing hepatic gluconeogenesis and increasing peripheral glucose uptake and glycogen storage. The molecular basis of this novel function of A20, as a positive regulator of glucose metabolism, likely relies on A20-induced modulation of liver-produced anti- vs. pro-diabetic solute carrier proteins (SLC) in a way that favors production and secretion of anti-diabetic (Lipocalin-13/LCN13), and reduces that of pro-diabetic Retinol binding protein 4/RBP4) SLC.