The transfer of miR-155 mediated by EVs from SMCs to endothelial cells, driven by KLF5, leads to the disruption of tight junctions and endothelial barrier integrity, promoting atherosclerosis.276 The transfer of miR-143 and miR-145 in endothelial cell EVs induced by KLF2 blocks the transdifferentiation of SMCs, thereby mediating a protective effect against atherosclerosis through endothelial cell-SMC communication.277. This evidence concerns the gene KLF5 and atherosclerosis.