In addition to the above-mentioned specific mutant of FOXA1 and FOXA2 in mouse pancreatic islets, mice lacking FOXA1 generated by homologous recombination in embryonic stem cells also exhibited persistent hypoglycemia and early postnatal death, etc. On the premise that pancreatic α and Β cells from mutant mice have been shown to differentiate normally, hypoglycemia in mice did not stimulate glucagon secretion, and its level paradoxically decreased. The gene discussed is FOXA1; the disease is Hypoglycemia.