Type 1 interferon (IFN) appears to play the critical role in mediating endothelial damage in patients with SLE [55], alongside with other endothelial toxic mediators and conditions both dependent and independent of type 1 IFN including proinflammatory cytokines, costimulatory molecules, immune complexes, oxidized lipid species, oxidative stress, autoantibodies, including antiphospholipid antibodies and anti-annexin-V antibodies, and the process of neutrophil extracellular traps (“Netosis”). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.