Nowadays therapy for ARDS remains mainly supportive, designed to prevent secondary injury [11] . However, recent studies demonstrated that organ damage in sepsis involves an alteration in gene expression. Decreased transcription of surfactant proteins [12] as well as profound pulmonary epithelial dysregulation together with altered levels of Hsp70 were found in animal models of ARDS [13] . We also showed in our previous studies that severe sepsis induced by cecal ligation and puncture (2CLP) precipitates ARDS [13, 14] . Furthermore, we demonstrated that enhanced Hsp70 expression in pneumocytes using an adenoviral vector (AdHSP) not only decreased histological abnormalities in the lung but also improved shortterm outcome [15] . Specifically, we showed that AdHSP limited sepsis-induced acute inflammation by suppressing NF-κB activation [50] .