JUN and periodontitis: Our in vivo data using a P. gingivalis–induced alveolar bone loss model also confirmed the anti-inflammatory role of SGK1-TRAF2/3–c-Jun/NF-κB signaling axis, suggesting that targeting SGK1-mediated TRAF signaling, or the expression of c-Jun, could be a novel strategy to manipulate the intensity and direction of inflammation and thus benefit patients with inflammatory diseases relevant beyond periodontitis.