Systemic lupus erythematosus (SLE) is a multifaceted autoimmune disorder that includes loss of tolerance to self-antigen and subsequent activation of autoreactive T and B cells, production of dysregulated cytokines (1), and the production of autoantibodies such as anti-phospholipid antibodies (anti-aPL) (2), anti-ribonucleoprotein antibodies (anti-RNP) (3), anti-double-stranded DNA (anti-dsDNA) (4), and anti-IgE (5), and circulating immune complexes which when deposited in organs activate complement cascades leading to tissue injury (6). This evidence concerns the gene FASLG and systemic lupus erythematosus.