It seems intuitive that in a disease marked by hyperglycemia, normalization of glycemia should prevent the end-organ damage associated with it. Indeed, lowering blood glucose has been the focus of diabetes management for decades on the presumption that it would improve risk of renal failure, cardiovascular events, and death in patients with elevated levels of glycated hemoglobin, even though the proof for such effect has been elusive.1 The United Kingdom Prospective Diabetes Study (UKPDS) appeared to validate the targeting of lower hemoglobin A1c (HbA1c) levels in type 2 diabetes, as this randomized trial showed lower rates of microvascular complications of diabetes such as retinopathy and renal failure in patients under intensive glycemic control compared with conventional therapy.2 However, a growing body of evidence supports the idea that intensive glycemic control causes harm in certain subpopulations of diabetic patients who were underrepresented in trials like the UKPDS. Consider that patients in the UKPDS were newly diagnosed and relatively healthy, with a mean age of 53 years. Those older than 65 years were excluded. Contrast this with the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, in which the upper age limit was 79 years and the mean age was 63 years. This trial was stopped early because of higher all-cause mortality in the intensive therapy group.3 Clearly, for this patient demographic, intensive glycemic control is risky business. Indeed, what was previously considered good control for all is now considered overtreatment in elderly patients because it is associated with more harm than benefit.