The most clear example of a potential site from in vivo study was the recent report using pharmacologic and genetic deletion and addition analyses in C57BL6 mice and endotoxin treatment (not sepsis), which clearly linked SIRT1 in CD11c dendritic cells to reprogram the axis between CD4+ Th1 cells and CD4+ TReg repressor cells [36]; these results parallel what may be occurring in this sepsis in this study, and mechanistically this path requires deacetylation of NF-κB p64 [5]. This evidence concerns the gene NFKB1 and Sepsis.