Recently it was shown that ACPA can cause platelet activation in vitro via FcγRIIa.[12] Given that ligand binding to FcγRIIa results in activation of the GPVI shedding pathway, we hypothesized that levels of sGPVI would be increased among patients with seropositive RA as a consequence of antibody induced platelet activation and GPVI shedding. Here, GP6 is linked to rheumatoid arthritis.