During human endotoxemia and sepsis, circulating Angpt1 levels remain unchanged or even decrease, whereas the endogenous context-specific Tie-2 antagonist, angiopoietin-2 (Angpt2), is rapidly released by the activated endothelium and disrupts the constitutive Angpt1/Tie2 signaling by preventing Angpt1 from binding to the receptor [12-19]. The gene discussed is TEK; the disease is Sepsis.