Activation of complement system by deposited ICs cause tissue damage, but, in the other hand, components of the classical pathway (CP) have a protective role in facilitating the clearance of ICs and apoptotic bodies, and their deficiency increases the risk of SLE [2,3], this association explained not only by ICs removal from circulation, but also by other mechanisms, including reduction of activation thresholds of lymphocytes and loss of self-tolerance [4,5]. This evidence concerns the gene CP and systemic lupus erythematosus.