ACPA can induce pain, bone loss, and inflammation in RA.47,48 One study has identified that two RA-specific autoantigens N-acetylglucosamine-6-sulfatase (GNS) and filamin A (FLNA) correlate microbial immunity with autoimmune responses in the joint.49 What is more, it has been proposed that citrullination plays a unique role during osteoclast differentiation and ACPA-induced osteoclast activation which might explain important features of the gradual development of RA including why the joints are targeted. This evidence concerns the gene PRTN3 and rheumatoid arthritis.