In our experimental model of advanced atherosclerosis and in patients with ACA, we observed a significant decrease in miR-143-3p whereas in ApoE−/− mice after only 8 weeks of HFD and in subjects with fibrolipidic plaques, both with early atherosclerosis, miR-143-3p levels did not significantly differ from their respective controls. The gene discussed is APOE; the disease is atherosclerosis.