Although the ATP-dependent potassium channel is one of the central players in glucose-stimulated insulin secretion, and altered potassium channel activity is related to the impaired insulin secretion in MODY patients [32], [33], there are contradicting data on whether or not one of its subunits, Kir6.2, is a direct target of HNF4α. The gene discussed is INS; the disease is MODY.