Background Krüppel-like transcription factor 2 (KLF2) has been identified as a key regulator of endothelial antithrombotic function.KLF2 was strongly implicated to be a novel nuclear mediator of statin effects in association between coronary risk factors and atherosclerotic disease burden measured by intravascular ultrasound endothelial cells.We hypothesized that rosuvastatin might induce the expression and activity of KLF2, thereby counteracting coronary endothelial dysfunction induced by DESs.