CD8A and systemic lupus erythematosus: SLE is a complex and heterogeneous autoimmune syndrome characterised by numerous abnormalities, including various autoantibodies, the appearance of unusual CD4-CD8- TCR-αβ+ cells, altered metabolism of lymphocytes, a type I interferon (IFN-I) gene signature in peripheral blood mononuclear cells (PBMC), increased formation of neutrophil extracellular traps (NETs), and deposition of immunoglobulins and complement at renal glomeruli.1–10 Each of these immune abnormalities may provoke different aspects of the disease, and each also may be driven by different environmental and genetic aberrations.