Protein Tyrosine Phosphatase 1B (PTP1B) and endoplasmic reticulum stress (ERS) are involved in the septic inflammatory response. Their inhibition is associated with improved survival in murine models of sepsis. In a recent publication in Frontiers in Medicine Dr Clavier et al showed in a study of 40 patients with septic shock that gene expression variation in blood samples of PTPN1 and ATF6 partly correlate with the evolution of septic organ failure and with markers of endothelial dysfunction. The recent identification of PTP1B as a novel negative regulator of host defense against sepsis may have potential therapeutic implications. However, further studies are needed to better understand PTP1B and ERS implication during sepsis in humans.