Mechanistically, NORAD causes endothelial cell senescence and apoptosis in atherosclerosis, mainly by manipulating the NF-κB and p53–p21 pathways and IL-8 expression, in which NORAD-mediated regulation of IL-8 expression may directly target splicing factor proline and glutamine rich (SFPQ). The gene discussed is CXCL8; the disease is atherosclerosis.