During sepsis, plasma antithrombin levels are markedly decreased because of consumption resulting from ongoing clotting activation, impaired synthesis and degradation by neutrophil proteases.11 The observation that inflammatory stimuli can down-regulate the expression of heparan sulphate proteoglycan in cultured ECs1,33 suggests an additional mechanism contributing to the reduced antithrombin function in sepsis. Here, GPC3 is linked to Sepsis.