We hypothesized that: (i) prolonged insulin-induced hypoglycaemia causes a compensatory decrease in β-cell insulin production and secretion accompanied by decreased overall mass of β-cells and pancreatic islets, (ii) following withdrawal of exogenous insulin, normal β-cell mass as well as insulin production and secretion will be re-established, and (iii) islet glucagon content will increase during hypoglycaemia and normalize after end of dosing. The gene discussed is INS; the disease is Hypoglycemia.