The significance of these findings is highlighted by the facts that currently there is no effective medication for the treatment of vasodilatory shock in patients with sepsis, and inhibition of the TNF/KLF4/Sp1/HDAC/CPI-17 signaling by genetic deletion of TNF or pharmacological inhibition of HDACs protects mice from LPS-induced hypotension, vascular hypocontractility, and mortality. Here, KLF4 is linked to Sepsis.