This is an important differentiation from human PAD genes (which endocitrullinate) as one of the proposed mechanisms in which P. gingivalis induces arthritis is via the release of the virulence factor arginine-gingipanis (RpgB) which cleaves host proteins exposing the terminal arginine residue which is then free to undergo citrullination via PPAD with the creation of neo-epitopes and subsequent ACPA positivity (Wegner et al., 2010). This evidence concerns the gene PRTN3 and arthritic joint disease.