The hyperactivation of complement was found to contribute to endothelial cell injury, thrombosis and intravascular coagulation, ultimately leading to multisystemic organ failure and excessive coagulation in COVID-19 patients.18,55,56 The potent anaphylatoxin C5a attracts neutrophils and monocytes to the infection site, causes tissue damage by oxidative radical formation and enzyme release, and leads to the activation of the coagulation system.43 These studies suggest that the coagulation-related symptoms in COVID-19 may also be associated with the abnormal activation of complement. The gene discussed is C5; the disease is COVID-19.