Because GLUT2 confers susceptibility to hyperglycemia-induced NTDs [5], and high glucose concentrations significantly inhibit GLUT2-transported GlcN [18], we hypothesized that the differences in susceptibility to diabetic embryopathy of FVB and B6 embryos is due to differential dependence on exogenous (maternal) GlcN to support hexosamine biosynthesis, promote growth, and regulate oxidative stress. This evidence concerns the gene SLC2A2 and Hyperglycemia.