In particular, Dr. Accili’s group [14] reported that genetic inactivation of FOXO1 transcription factor in mice resulted in the expansion of NGN3-positive enteroendocrine progenitor cells, and appearance of functional insulin-producing cells that expressed all markers of mature β-cells, secreted insulin in response to glucose and sulfonylureas, and could alleviate diabetes caused by streptozotocin. The gene discussed is INS; the disease is diabetes mellitus.