Besides, KLF4 was found to cooperate with Stat6 to induce an M2 genetic program and inhibit M1 targets via sequestration of coactivators required for NF-κB activation, which suggested KLF4 to be a novel regulator of macrophage polarization [29] and the treatment of atherosclerosis [26,27]. This evidence concerns the gene NFKB1 and atherosclerosis.