While in humans, it was reported that the sera of 3MC syndrome patients deficient for both MASP-1 and MASP-3 lacked C4 deposition activity on mannan via the LP but exhibited lowered hemolytic activity via the AP (33, 34), suggesting the existence of a backup system that activates pro-FD at least in humans. The gene discussed is C4A; the disease is 3MC syndrome.