Overexpression of miR-30c was found to reduce plaque formation in the atherosclerosis prone apolipoprotein E (Apo E) deficient mouse model, while inhibition of miR-30c caused severe hyperlipidemia and atherosclerotic plaque formation, thus suggesting that also miR-30c mimetics may be a promising therapeutic approach in patients at risk of CVDs [63]. This evidence concerns the gene APOE and atherosclerosis.