In addition, when we analysed the transition from IGT to diabetes, we observed an additional reduction in the expression of NKX6.1 and MAFA. This confirms previous in vitro findings in diabetic individuals with a downregulation of FOXO1, which suggests the impaired capacity of type 2 diabetic islets to compensate for metabolic requirements and a final propensity to acquire a dedifferentiated phenotype [29–32]. The gene discussed is FOXO1; the disease is diabetes mellitus.