The possible reasons for statin-mediated suppressive effects on endothelial dysfunction are partially due to increased KLF2 expression and regulation of the expression of its downstream genes, which include NF-kB-dependent pro-inflammatory genes (VCAM-1, SELE and CCL2), thrombotic genes (THBD and THBS1) and vascular homeostasis-associated genes (eNOS and ET1). The gene discussed is CCL2; the disease is endothelial dysfunction.