Concerning fibrinogen abnormalities, most of our patients were carriers of the frequent mutations in FGA exon 2 (p.Arg35Cys and p.Arg35His) or in FGG exon 8 (p.Arg301His), which are responsible for more than 80% of all variants in dysfibrinogenemia [67]. Here, FGG is linked to familial hypodysfibrinogenemia.