During sepsis, a variety of promoters of FXII activation (Fig 9, panel 4), including poly-P [34] and nucleic acids from microorganisms and damaged tissues [36,37], plasmin generated during hyperfibrinolytic responses [54,55], and bacterial surfaces [56,57] could induce contact activation leading to FXI activation and, ultimately, to increased thrombin production. The gene discussed is F11; the disease is Sepsis.