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 The gene discussed is INS; the disease is type 2 diabetes mellitus.