LPS derived from P. gingivalis have been shown to promote the secretion of periodontal disease‐related proinflammatory cytokines by PDLFs.13 LPS are also involved in RANKL and OPG‐regulated osteoclast formation and bone resorption in PDLFs,14 and their inhibitory effect on the osteoblastic differentiation of osteoprogenitor cells.15 LPS are thus believed important pathogens in periodontitis that can lead to alveolar bone resorption in most advanced cases. The gene discussed is TNFSF11; the disease is periodontal disorder.