Corroborating the animal and some in vitro data, type-I IFN signatures or high serum IFN-α are associated with accelerated endothelial cell apoptosis, impaired endothelial progenitor cell (EPC) function, reduced flow-mediated dilation, increased foam cell formation, enhanced pro-inflammatory leukocyte recruitment, platelet activation with subsequent thrombosis and elevated endothelial activation markers in systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS) and rheumatoid arthritis (RA) [25,26,27]. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.