Angiotensin-converting enzyme (ACE) inhibitors are recommended for all patients with type 1 diabetes and microalbuminuria, regardless of blood pressure (1). These recommendations are based on well-conducted clinical trials (2), but several questions remain unanswered. First, the range of renal disease included in studies of patients with microalbuminuria is broad, from relatively high albumin excretion rates associated with advanced renal disease to mild elevations of albumin excretion rate and relatively normal glomerular structure. Because microalbuminuria often occurs in the first 5 years after diagnosis (3), relatively young people may begin therapy with ACE inhibitors on the basis of this indication alone and would be expected to continue taking these drugs indefinitely. Furthermore, in several of these trials, change in albumin excretion rate is used as a surrogate end point, with the implicit assumption that it indicates progressive renal disease. A demonstration that ACE inhibitors reduced the risk for progression to a more definite end point, such as clinical proteinuria, would add support to intervention strategies. Although some studies have reported a statistically significant effect of ACE inhibitors on progression to macroalbuminuria (4–5), most were not adequately powered to do so. For example, if the risk for progression to macroalbuminuria in the placebo group is assumed to be 20% over a 2-year period, 147 patients in each group would be required to detect a relative risk of 0.33 with a power of 0.9 power and a significance of 0.05. No study has yet reported the risk for regression to normoalbuminuria, and published individual studies are not powered to do so.