NFKB1 and Sepsis: During the transition from hyper- to hypo-inflammation, an increase in nuclear NAD+ activates SIRT1, which supports the regulation of the key inflammatory genes such as TNF-α and IL-1β through NFκB p65 deacetylation, indicating the central role played by SIRT1 in the regulation of immune-suppression during sepsis [36,187,188].