Inhibition of the miR-103-KLF4 interaction reduced atherosclerosis, lesional macrophage accumulation and endothelial CXCL1 expression in the arteries of Apoe−/− mice, indicating a proinflammatory and proatherogenic role of miR-103 by targeting KLF4. The gene discussed is CXCL1; the disease is atherosclerosis.