As KLF4 is a negative regulator of contractile genes, the modulation of the miR-128-3p/KLF4 axis by LINC01005 in ox-LDL-treated HUVEC-derived exosomes reduces contractile markers such as α-SMA and SM22, and induces synthetic SMC markers such as OPN, which promote the synthetic phenotype of VSMCs and consequently induce atherosclerosis [58,59]. This evidence concerns the gene KLF4 and atherosclerosis.