C3a and C5a, which are known as anaphylatoxins, are pleiotropic inflammatory mediators.[35] The complement cascade is controlled by several soluble membrane-bound factors, including CD59, which inhibits the complement pathway at the feto-maternal interface.[36] In a model of spontaneous abortion, C3a and C5a were shown to be required for triggering abortion; C5a in particular was found to be critical for the induction of abortion.[37] Our data were also consistent with those of previous studies in humans investigating C3a, C5a and CD59 levels. The gene discussed is C3; the disease is abortion.