Effective anti-Porphyromonas immune responses in pre-clinical RA could explain the observed depletion of Porphyromonas once RA is established, especially in people carrying the functional PAV allele, whereas persistent periodontal inflammation could contribute to the persistent elevated ACPA responses seen in RA with periodontal disease, and possibly RA disease activity seen with periodontal disease. The gene discussed is PRTN3; the disease is rheumatoid arthritis.