In vivo preclinical data suggest that in C3 or C5‐deficient mice, the effect of aPL antibody‐mediated thrombosis is attenuated in the same way as with a C5 inhibitor in wild‐type mice, suggesting that complement may be activated in patients with aPL antibodies resulting in excessive generation of C5a (which induces neutrophil and monocyte tissue factor‐dependent procoagulant activity as well as platelet aggregation and activation) [51]. This evidence concerns the gene C5 and Venous thrombosis.