The contact activation pathway’s relevance for maintaining hemostatic capacity in vivo has been debated as patients deficient in factor (F) XII, PK (pre-kallikrein), or HK (high molecular weight kininogen) do not typically present with a bleeding phenotype, and Factor XI (FXI) deficiency (hemophilia C), is a mild- to- moderate, tissue-specific bleeding disorder. The gene discussed is KNG1; the disease is congenital factor XI deficiency.