Deficiencies in complement are associated with auto-immune diseases such as systemic lupus erythematosus (SLE), frequently seen in defects of the early components of the classical pathway (C1Q, C1R/S, C2, C4) or with susceptibility to meningococcal disease and/or atypical hemolytic uremic syndrome (aHUS) by defects in the terminal pathway components (C5, C6, C7, C8A/B/G, C9) or complement regulators (CFP, CFH, CFD, CFI, CD46). This evidence concerns the gene CFD and systemic lupus erythematosus.