CCN1 increases the expression of oncostatin M in human osteoblastic cells [26], synthesizes pro-IL-1β and enhances the expression of MMP-3 in human RA FLS [31], promotes FLS proliferation and participates in RA pathogenesis via the IL-17-dependent pathway [49] and also promotes the expression of CCL2 and monocyte migration by inhibiting miR-518-5p expression in osteoblasts via mitogen-activated protein kinase (MAPK) signaling [11]. Here, IL17A is linked to rheumatoid arthritis.