Crippling of Krüppel (-like factor 2) by bad flow portends a miRky day for endothelial function.

Krüppel-like Factor 2 (KLF2) is a 38-kDa transcription factor that is highly expressed in the vascular endothelium. The enormous attention that KLF2 has received in recent years is well deserved, because experimental evidence has shown that it is a vital protein that, via transcriptional and nontranscriptional targets, mediates a host of endothelial functions.1 These include inhibition of vascular inflammation and attendant atherosclerosis, maintenance of an antithrombotic endothelial surface, stimulation of endothelial nitric oxide synthase expression and vascular nitric oxide production, inhibition of hypoxia-stimulated angiogenesis, and promotion of prenatal vasculogenesis, among others. It is not surprising, therefore, that regulation of endothelial KLF2 expression has been the subject of intense investigation.