Although our cohort size was small, the production of autoantibodies, particularly ACPA, is a key feature in RA, and they serve as important diagnostic and prognostic indicators.22 Recently, direct functional activities mediated by ACPA—for example, via FcR dependent pathways, and osteoclast maturation via citrullinated-vimentin recognition have attracted increasing attention.24 Importantly, we now demonstrate that anti-MICL antibodies can exacerbate disease, at least in murine models, suggesting a new means whereby resolution can fail and myeloid-dependent inflammation can prevail. This evidence concerns the gene VIM and rheumatoid arthritis.