Considering the role of miR-155 deficiency in ApoE−/− mice that resulted in advanced atherosclerosis, we therefore hypothesized that this miR-155 inhibition induced by the genetic variant could reduce macrophage migration and atherosclerosis progression and therefore decreased the risk of plaque rupture during advanced atherosclerosis and prevented patients from SCD. The gene discussed is APOE; the disease is Schnyder corneal dystrophy.