Patients with septic shock are characterized by high rates of organ failure and mortality.1 Dysfunction of the endothelium, the inner lining of blood vessels, referred to as endotheliopathy, may be important in the pathophysiology of septic shock.2,3,4,5 Shock-induced endotheliopathy can be assessed by soluble thrombomodulin (sTM) and has been independently associated with worsened organ failure and mortality in adult intensive care unit (ICU) patients with sepsis.3,6,7,8. The gene discussed is THBD; the disease is septic shock.