Activation of the alternative complement can be caused by infectious agents, malignancy, bone marrow or solid organ transplantation and chemotherapeutic or immunosuppressive agents [4,5], systemic illness (systemic lupus erythematous, membranoproliferative glomerulonephritis, antiphospholipid antibody syndrome, scleroderma) [6,7], severe pre-ecclampsia [8], hyperhomocystinemia [9,10], mutations in the thrombomodulin (THMB) [11] or diacylglycerol kinase ε (DGKE) gene [12]. Here, THBD is linked to Hyperhomocystinemia.