Several pathophysiological hypotheses could explain these results, including reduced ACE activity, as shown in experimental sepsis or pediatric septic shock [12, 13] or increased degradation of Ang II, either by ACE2 or by peptidases, such as circulating dipeptidyl peptidase 3 (cDPP3) [11, 14, 15, 16, 17]. This evidence concerns the gene DPP3 and Sepsis.