In addition, SGK1 inhibition aggravates P. gingivalis–induced periodontal inflammation in mice gingiva and exacerbates subsequent alveolar bone loss, suggesting that the anti-inflammatory signaling axis, SGK1–TRAF2/3–c-Jun/NF-κB, could be targeted for the development of novel interventional therapeutics to control periodontitis and other inflammatory diseases beyond the oral cavity. The gene discussed is JUN; the disease is periodontitis.