The main findings of our study were that (a) BML-111 reduced the level of neuroinflammation, activation of glias, number of TUNEL-positive cells, and cognitive impairment induced by sepsis, and (b) the underlying mechanism was activation of SIRT1 by BML-111 followed by suppression of the NF-κB activation. Here, NFKB1 is linked to Sepsis.