Complement-related disorders—like C3 glomerulopathy (C3G), paroxysmal nocturnal hemoglobinuria (PNH), and atypical hemolytic uremic syndrome (aHUS)—are attributed to inappropriately regulated complement activation and are often strongly associated with mutations in key complement regulatory proteins, like factor H, CD46, CD55, and/or CD59 [7,8,11]. This evidence concerns the gene CD59 and complement 3 glomerulopathy.