Indeed, mice with OGT-KO in pancreatic β-cells develop severe diabetes due to β-pancreatic insufficiency associated with decreased expression of insulin genes (ins1 and ins2) and transcription factors controlling these genes (Pdx-1 and NeuroD1), decreased PI3K/Akt pathway activity, and β-cell apoptosis induced by endoplasmic reticulum stress [72]. The gene discussed is OGT; the disease is diabetes mellitus.