In contrast, dysfunctional HDL derived from CAD patients delivered miR-24-3p via SR-B1, inhibiting vinculin expression and NO production, and leading to superoxide production, while the overexpression of vinculin or inhibition of miR-24-3p reversed the impaired angiogenesis associated with dysfunctional HDL [189]. This evidence concerns the gene VCL and coronary artery disorder.