In mature β cells, FoxO1 is localized in the cytoplasm, then shuttling to the nucleus depending on the metabolic status of the cell, in order to maintain the expression of specific transcription factors such as PDX1, NKX6.1 and MafA. However, chronic hyperglycaemia causes FoxO1 degradation, leading to decreased insulin content and upregulation of genes associated to the endocrine progenitor phenotype, such as Vimentin (mesenchymal marker), Ngn3 (endocrine progenitor marker), OCT4, Nanog or L-MYC (stem cell markers) [20]. The gene discussed is FOXO1; the disease is Hyperglycemia.