Importantly, in the absence of hyperglycaemia, the number of apoptotic cells in the pancreatic islets was not different between vehicle and TAM-treated mice, which was corroborated in Glis3-knockdown INS-1 derived 832/13 cells, indicating that the increased apoptosis that occurred after onset of hyperglycaemia was a consequence of glucotoxicity and not a direct effect of loss of Glis3 expression. The gene discussed is GLIS3; the disease is Hyperglycemia.