Using the mouse atherosclerosis models of ApoE–/– and LDLR–/–, a study found that miR-181b inhibition substantially increased elastin and collagen expression levels through negative regulation of downstream target TIMP-3 expression and promoted a fibrotic response and consequent stabilization of existing plaques or aneurysms (Di Gregoli et al., 2017). This evidence concerns the gene ELN and atherosclerosis.