The pathogenesis of PF and SPG in patients with severe systemic infections is not well understood, but is thought to involve a decrease in the synthesis of physiologic anticoagulants PC, PS, or antithrombin III (AT3) [5,7], particularly in the context of ischemic hepatitis or “shock liver.” Patients with severe sepsis and septic shock have been shown to have decreased levels of PC and AT3, with the degree of reduction in protein C concentration directly correlated with the severity of sepsis [9]. The gene discussed is SERPINC1; the disease is septic shock.