Furthermore, EV-associated miR-92a released by ECs in response to atheroprone stimuli was demonstrated to suppress the expression of target gene KLF4 (Krüppel-like factor 4) in macrophages, suggesting a mechanism by which EV-associated miR-92a regulates the pro-inflammatory phenotypes of macrophage and, hence, atherosclerotic lesion formation 78, an effect observed also with large EVs from patients with coronary artery disease 79. This evidence concerns the gene KLF4 and coronary artery disorder.