Moreover, in mouse models of LPS-induced sepsis, SRT1720 significantly reduced LPS-induced lung injury by limiting hyperpermeability through the reduction in reactive oxygen species production and SIRT1-dependent suppression of NF-κB–mediated inflammation with preservation of tight junction proteins, thereby reducing endothelial permeability [30,31], and by reducing LPS-induced macrophage apoptosis through the inhibition of the endoplasmic reticulum stress response [11]. The gene discussed is NFKB1; the disease is Sepsis.