While the cellular origin of the high levels of sDLL1 observed in our patients with sepsis remains speculative, the mechanism of formation is known: transmembrane DLL1 is cleaved by a combined ADAM protease and γ-secretase activity upon binding to Notch receptor and therefore, sDLL1 is a surrogate of recent Notch signaling (Six et al., 2003; Dyczynska et al., 2007). This evidence concerns the gene DLL1 and Sepsis.