Further studies with large sample size of patients for measurements of complement component protein levels under defined genetic backgrounds, plus determination of activation products C3a, C4a, and C5a, cell-bound and fluid phase levels of C4d and C3d, and membrane attack complexes may provide important insights into mechanism(s) on how complement modulate aPL associated clinical manifestations and disease activities of SLE and APS (55, 58, 61, 62). Here, C5 is linked to autoimmune polyendocrinopathy.