Banda et al. [27] demonstrated the key role of MASP-3 (unbound or associated with ficolin-B but not with MBL-A or MBL-C) in the cleavage of profactor D, and MASP-1/3-deficient mice were protected from arthritis development [38, 52], whereas disease activity was decreased in MASP-2−/−/sMAp−/− animals [26]. The gene discussed is FCN2; the disease is Arthritis.