KEAP1 and periodontitis: Findings from recent studies have reported an emerging molecule, four-octyl itaconate (4-OI) that activates Nrf2 pathway by alkylating KEAP1’s key cysteine residues to disassociate KEAP1-Nrf2, has been utilized for controlling many inflammatory diseases, such as sepsis and acute lung injury.26–28 Intracellularly, esterase and lipopolysaccharide (LPS)-activated macrophages hydrolyze 4-OI to form itaconate, making it a cell-permeable substitution for itaconate.26 However, the potential activity of 4-OI in the treatment of periodontitis has never been studied.