The findings that inhibition of the interaction between miR-103 and KLF4 reduced atherosclerosis and increased endothelial KLF4 expression in Apoe−/− mice demonstrates a proatherogenic role of this interaction and suggests that derepression of KLF4 due to downregulation of miR-103 contributes to the atheroprotective effect of Dicer deficiency in ECs. This evidence concerns the gene APOE and atherosclerosis.