We observed significant downregulation of Mafa, Ins1, and Ins2 mRNAs, and significant upregulation of Aldob, Slc5a10, Wnt5b, Hk1, and Tnfrsf11b mRNAs, suggesting that the molecular defect results directly from the loss of Cnot3, rather than to hyperglycemia (Supplementary Fig. 12). This evidence concerns the gene TNFRSF11B and Hyperglycemia.