The underlying mechanism is that they can inhibit the accessibility of NF-κB with its cofactors, including p300 and p300/CBP-associated factor (PCAF), on the promoters of inflammatory genes.213 Ganapati H Mahabeleshwar et al. revealed that macrophage-specific KLF2-knockout mice are sensitive to sepsis and a robust inflammatory response and demonstrate enhanced pathogen clearance in models of bacterial peritonitis.213 On the contrary, KLF4 directly interacts with critical M2 transcription factor STAT6 to induce the transcription of M2 genes. This evidence concerns the gene NFKB1 and Sepsis.