Thus, the hPSC model for HNF6 deficiency helped to understand that the resultant diabetes is caused by diminished interaction of the ONECUT1 C terminus with NKX6.1/NKX2.2 and a reduced chromatin accessibility during transition from posterior foregut to pancreatic progenitors which in turn regulates development of adequate mass. This evidence concerns the gene NKX2-2 and diabetes mellitus.