PNH is associated with the loss of two complement-inhibiting surface proteins (CD55 and CD59) expressed mainly on the surface of red blood cells and leading to a dysregulated complementary activation that results in hemolysis and thrombosis [95]: VTE events are common, affecting 29–44% of the subjects, and associated with an increased mortality. The gene discussed is CD59; the disease is paroxysmal nocturnal hemoglobinuria.