Jiang et al., reported that in an LPS- and ligature-induced periodontal disease rat model, BTZ suppressed the expression of TNF-α, IL-1β, IL-6, and IL-8; reduced the ratio of receptor activation of RANKL/osteoprotegerin; and prevented alveolar bone resorption, suggesting that the anti-inflammatory activity of BTZ has a promising therapeutic effect against periodontal inflammatory responses in periodontal disease [65]. The gene discussed is TNFRSF11B; the disease is periodontal disorder.