Finally, complement activation contributes to early and late phases of coagulopathy: MASP-1, MASP-2, and thrombin promote D-dimer elevation, thrombocytopenia, and prolonged PT in early disease, while later MASP-1-driven activation of prothrombin and fibrinogen leads to widespread thrombosis and fibrin degradation [31]. The gene discussed is MASP1; the disease is Thrombocytopenia.