Subsequently, Ago2 dissociates from the miR-126 in the nucleus, allowing miR-126 to bind to caspase-3.[10] Dysfunctional efferocytosis and the accumulation of apoptotic endothelial and foam cells collectively accelerate atherosclerotic plaque formation.[71] These findings indicate that Ago2 may play a protective role against atherosclerosis. The gene discussed is AGO2; the disease is atherosclerosis.