Mechanistically, due to stress resulting from glucotoxicity, lipotoxicity, or inflammation in diabetes β-cells degenerate from their mature differentiated state to a dedifferentiated state through (1) the downregulation of β-cell-enriched genes (such as Glut2, Pdx1, Foxo1, and MafA), (2) upregulation of β-cell-forbidden genes such as hexokinase [HKI-III] or Ldha, and (3) induction of progenitor cell-associated genes such as Neurogenin 3 [Ngn3], L-Myc, Nanog Homeobox [Nanog] octamer-binding transcription factor [Oct4], and POU domain class 5 transcription factor 1 [Pou5f1] [12,13]. This evidence concerns the gene NEUROG3 and diabetes mellitus.