In the context of periodontal disease, this effect of AaCdt provides a molecular mechanism by which Aa functions in the oral cavity to provide a “survival” niche in the gingival crevice for other pathogenic microorganisms which collectively contribute to LAP pathogenesis (Loe and Brown, 1991; Teughels et al., 2014; Fine et al., 2019). The gene discussed is TEAD1; the disease is periodontal disorder.