Hyperglycaemia paradoxically impacts insulin secretion by causing temporary β-cell ‘paralysis’, a phenomenon known as glucotoxicity.29 Early insulin can help overcome the glucotoxicity effects of hyperglycaemia by preserving β-cell mass and function.29 Therefore, depending on the duration ± degree of β-cell failure, exogenous insulin can successfully be discontinued in many patients with T2DM by addressing glucotoxicity and optimising lifestyle and other antihyperglycaemic agents.30 This evidence concerns the gene INS and Hyperglycemia.