Furthermore, IL-17A gene transfer to C57BL/6 J mice in a collagen-induced arthritis (CIA) model of inflammatory arthritis showed elevated levels of IL-17RA+CD11b+Gr1lowRANK+CSF-1R+ osteoclast precursors with increased differentiation capacity compared to precursors from control mice even before arthritis onset, suggesting that IL-17A expression may exacerbate bone destruction even in the absence of inflammation [173]. This evidence concerns the gene IL17A and arthritic joint disease.