It is characterized by nonfunctional glucose transporter 2 (GLUT2) mutation, hepato-renal glycogen accumulation, both fasting hypoglycemia as well as postprandial hyperglycemia and hypergalactosemia indicating an impaired utilization of these two monosaccharides, and proximal renal tubular dysfunction [6, 7]. This evidence concerns the gene SLC2A2 and Hyperglycemia.