In 1994, a study in Xenopus oocytes proved that a highly conserved GLUT2 missense mutation in one allele of the gene (substituted Val197 to Ile197) leads to GLUT2 dysfunction, and might be expected to play an important role in pathogenicity of non-insulin dependent diabetes mellitus [4,5]. This evidence concerns the gene SLC2A2 and type 1 diabetes mellitus.