Finally, technical details such as a role for the small remaining Syk expression after Cre-mediated Syk deletion, or different experimental conditions may also account for the different conclusions drawn from our study and from those proposing a critical role for the platelet GpVI–FcRγ–Syk pathway in autoantibody-induced arthritis (10, 33). This evidence concerns the gene FCER1G and arthritic joint disease.