As for dysfibrinogenemias and hypodysfibrinogenemias, these disorders are usually inherited as an autosomal dominant trait: they are caused by a single genetic defect ultimately affecting a functional property of the fibrinogen protein, such as the release (impaired or delayed) of fibrinopeptides A and B, defective polymerization, crosslinking, or thrombin binding, as well as delayed plasmin digestion [16]. The gene discussed is FGA; the disease is familial hypodysfibrinogenemia.