In SLE, complements have a biphasic nature, which is known as the “lupus paradox [11].” That is, complement activation via immune complexes deposited in tissues causes tissue damage, whereas congenital deficiencies of the early components of complement activation pathways, such as C1q and C4, which are involved in the processing of apoptotic cells, frequently lead to the development of SLE [12]. The gene discussed is C4A; the disease is systemic lupus erythematosus.