In the early stages of toll-like receptor 4- (TLR4-) mediated sepsis, SIRT1 rapidly accumulated at TNF-α and IL-1β promoter regions and deacetylated the RelA/p65 lysine 310 site and nuclear histone H4 lysine 16 sites, ultimately promoting NF-κB transcription termination. This evidence concerns the gene TLR4 and Sepsis.